The purpose of this study was to evaluate the shear bond strengths between various hybrid computer-aided design (CAD)/computer-aided manufacturing (CAM) restorative materials and repairing resin. Two resin network-based hybrid (Lava Ultimate and Polyglass), one ceramic framework-based hybrid (Enamic), and one zirconia (Zenotec Zr bridge) CAD/CAM restorative materials were used in this study. The shear bond strength test and failure modes of four experimental groups designated LUS (Lava Ultimate), ENA (Enamic), PGB (Polyglass), and ZBR (zirconia control group) were characterized in this study. The hybrid CAD/CAM restorative materials showed stronger shear bond strengths in the sequence of PGB, LUS, and ENA (P < 0.05). The shear bond strengths of PGB and LUS groups showed significantly higher than those of ZBR (P < 0.05), while ENA did not show any significant difference from ZBR (P < 0.05). The PEG and LUS groups mostly exhibited cohesive failure, but the ENA and ZBR groups predominantly showed adhesive failure. Therefore, resin network-based hybrid CAD/CAM restorative materials such as Lava Ultimate and Polyglass should be more useful for intra-oral repairs.
Adhesives ; Ceramics ; Composite Resins ; Computer-Aided Design ; Prostaglandins B

PURPOSE: In this study, the medication effects of Milnacipran and Pregabalin, as well known as fibromyalgia treatment medicine, in fibromyalgia syndrome patients were compared through the change of BOLD signal in pain related functional MRI. MATERIALS AND METHODS: Twenty fibromyalgia syndrome patients were enrolled in this study and they were separated into two groups according to the treatment medicine: 10 Milnacipran (MLN) treatment group and 7 Pregabalin (PGB) treatment group. For accurate diagnosis, all patients underwent several clinical tests. Pre-treated and post-treated fMRI image with block-designed pressure-pain stimulation for each group were obtained to conduct the statistical analysis of paired t-test and two sample t-test. All statistical significant level was less than 0.05. RESULTS: In clinical tests, the clinical scores of the two groups were not significantly different at pre-treatment stage. But, PGB treatment group had lower Widespread Pain Index (WPI) and Brief Fatigue Inventory (BFI) score than those of MLN treatment group at post-treatment stage. In functional image analysis, BOLD signal of PGB treatment group was higher BOLD signal at several regions including anterior cingulate and insula than MLN treatment group at post-treatment stage. Also, paired t-test values of the BOLD signal in MLN group decreased in several regions including insula and thalamus as known as 'pain network'. In contrast, size and number of regions in which the BOLD signal decreased in PGB treatment group were smaller than those of MLN treatment group. CONCLUSION: This study showed that MLN group and PGB group have different medication effects. It is not surprising that MLN and PGB have not the same therapeutic effects since these two drugs have different medicinal mechanisms such as antidepressants and anti-seizure medication, respectively, and different detailed target of fibromyalgia syndrome treatment. Therefore, it is difficult to say which medicine will work better in this study.
Antidepressive Agents ; Diagnosis ; Fatigue ; Fibromyalgia* ; Follow-Up Studies* ; Humans ; Magnetic Resonance Imaging* ; Prostaglandins B ; Thalamus ; Pregabalin

PURPOSE: Interleukin 6 (IL-6) and IL-8 participate in the pathogenesis of chronic rhinosinusitis with nasal polyps, and their levels are increased by prostaglandin E2 (PGE2) in different cell types. The purposes of this study were to determine whether PGE2 has any effect on the increase in the levels of IL-6 and IL-8 in nasal polyp-derived fibroblasts (NPDFs) and subsequently investigate the possible mechanism of this effect. METHODS: Different concentrations of PGE2 were used to stimulate NPDFs at different time intervals. NPDFs were treated with agonists and antagonists of E prostanoid (EP) receptors. To determine the signaling pathway for the expression of PGE2-induced IL-6 and IL-8, PGE2 was treated with Akt and NF-kappaB inhibitors in NPDFs. Reverse transcription-polymerase chain reaction for IL-6 and IL-8 mRNAs was performed. IL-6 and IL-8 levels were measured byenzyme-linked immunosorbent assay (ELISA). The activation of Akt and NF-kappaB was evaluated by western blot analysis. RESULTS: PGE2 significantly increased the mRNA and protein expression levels of IL-6 and IL-8 in NPDFs. The EP2 and EP4 agonists and antagonists induced and inhibited IL-6 expression. However, the EP4 agonist and antagonist were only observed to induce and inhibit IL-8 expression level. The Akt and NF-kappaB inhibitors significantly blocked PGE2-induced expression of IL-6 and IL-8. CONCLUSIONS: PGE2 increases IL-6 expression via EP2 and EP4 receptors, and IL-8 expression via the EP4 receptor in NPDFs. It also activates the Akt and NF-kappaB signal pathways for the production of IL-6 and IL-8 in NPDFs. These results suggest that signaling pathway for IL-6 and IL-8 expression induced by PGE2 might be a useful therapeutic target for the treatment of nasal polyposis.
Blotting, Western ; Dinoprostone* ; Fibroblasts* ; Interleukin-6* ; Interleukin-8* ; Nasal Polyps ; NF-kappa B ; Prostaglandins E ; RNA, Messenger ; Signal Transduction

OBJECTIVE: Nuclear factor kappa B (NF-kappa B) is a transcriptional factor in the expression of cyclooxygenase 2 (COX-2), the key enzyme in production of prostaglandins. The purpose of this study was to investigate the activation of NF-kappa B in human gestational tissues obtained from term pregnant women by various inducers. METHODS: Myometrium, chorion, and amnion were collected during cesarean section from term pregnant women not in labor. Cells from gestational tissues were isolated and cultured with Interleukin-1beta (IL-1beta), Tumor Necrosis Factor-alpha (TNF-alpha) or Lipopolysaccharide (LPS). The activation of NF-kappa B in cells of each tissues was measured by luciferase assay. RESULTS: Luciferase activity analysis showed significantly higher activity of NF-kappa B in myometrial cells treated with LPS, in chorion cells treated with IL-1beta and TNF-alpha, and in amnion cells treated with IL-1beta and LPS than control. CONCLUSION: In cells of gestational tissue at term pregnancy, the activation of NF-kappa B is cell-specific and various according to inducers.
Amnion ; Animals ; Cesarean Section ; Chorion ; Cyclooxygenase 2 ; Cytokines ; Female ; Humans ; Interleukin-1beta ; Luciferases ; Mice ; Myometrium ; NF-kappa B* ; Pregnancy ; Pregnant Women ; Prostaglandins ; Tumor Necrosis Factor-alpha

The use of ophthalmic drugs and contact lens solutions has increased and allergic contact dermatitis due to these agents has also recently increased. The first case was a 67-year-old female patient who developed allergic contact dermatitis after application of Latano(R): The patch test with the ingredients in Latano(R) showed positive reaction to latanoprost and benzalkonium chloride. The second case was a 63-year-old female patient who developed allergic contact dermatitis after application of Ecolicin(R), Tolon(R), Forus(R) and Uniten-F(R): The patch test showed a positive reaction to Tolon(R). She didn't want further evaluation. The third case was a 51-year-old female patient who developed allergic contact dermatitis after application of Terramycin(R) eye ointment: the patch test with the ingredients of Terramycin(R) eye ointment showed a positive reaction to polymyxin B. When contact dermatitis occurs in periorbital areas, topical ophthalmic ointment or lens cleanser needs to be considered as a causative agent.
Aged ; Benzalkonium Compounds ; Contact Lens Solutions ; Dermatitis, Allergic Contact ; Dermatitis, Contact ; Eye ; Female ; Humans ; Middle Aged ; Patch Tests ; Polymyxin B ; Prostaglandins F, Synthetic

Purpose: Cyclooxygenase (COX) is an enzyme that catalyzes the conversion of arachidonic acid to prostaglandins. The inducible form, COX-2, is induced by such proinflammatory and mitogenic stimuli as cytokines and growth factors, and it's expressed in inflamed tissues as well as neoplastic tissues. In addition, COX-2 inhibitors have been tried as chemopreventive agents in tumors. In order to elucidate the mechanisms of COX-2 inhibitors in human breast cancer, the effects of celecoxib, a well-known selective COX-2 inhibitor, on cell death in human breast MDA-MB-468 cancer cells were investigated. METHODS: Cell viability assay, PI staining, DNA fragmentation assay and western blot analysis were performed after treatment with celecoxib. RESULTS: Cell survival, as measured by MTT assay, was decreased by the treatment with celecoxib in a dose-dependent manner (IC50=50 micrometer). The sub-G1 fractions, analyzed by flow cytometry, and the DNA fragmentations were increased in a dose-dependent manner, suggesting that celecoxib induces apoptotic cell death in MDA-MB-468 cells. Celecoxib resulted in a decrease in the levels of COX-2 protein in a time-depended and dose-dependent manner. To investigate the mechanisms of celecoxib-induced apotosis, the activation of MAPK, NF-kB and Akt was analyzed by Western blotting. The treatment with celecoxib induces an increase in JNK phosphorylation and IkB degradation and a decrease in Akt phosphorylation. CONCLUSION: These results suggest that celecoxib-induced apoptosis is mediated through the signal transduction pathways associated with JNK, Akt and NF-kB in human breast cancer MDA-MB-468 cells.
Apoptosis ; Arachidonic Acid ; Blotting, Western ; Breast Neoplasms* ; Breast* ; Celecoxib ; Cell Death ; Cell Survival ; Cyclooxygenase 2 Inhibitors ; Cyclooxygenase 2* ; Cytokines ; DNA ; DNA Fragmentation ; Flow Cytometry ; Humans* ; Intercellular Signaling Peptides and Proteins ; NF-kappa B ; Phosphorylation ; Prostaglandin-Endoperoxide Synthases ; Prostaglandins ; Signal Transduction

PURPOSE: Overexpression of COX-2, an enzyme responsible fro the synthesis of prostaglandins, is well linked to human chronic lung diseases. The mechanism by which COX-2 expression is increased or enhanced in cancer cells remains largely unknown. Any compound which can reduce COX-2 expression may be considered as an anti-cancer agent. MATERIALS AND METHODS: Leptomycin B (LMB) is a metabolite of Streptomyces and a specific inhibitor of CRM1 nuclear export receptor. A549 is a human lung cancer cell line. To evaluate the effect of LMB on COX-2 expression induced by IL-1beta, a pro-inflammatory cytokine, in A549 cells, Western blot and RT-PCR assays were applied to measure COX-2 protein and mRNA expressions in response to IL-1beta, respectively. Luciferase experiments were done to measure promoter activity of COX-2, NF-kappaB or AP-1. CRM1 siRNA trasfection experiment was performed to knock-down endogenous CRM1. Biochemical protein fractionation method was also carried out to see intracellular localization of proteins. RESULTS: LMB at 9 nM strongly suppressed IL-1beta-induced expression of COX-2 protein that was attributable to decreased COX-2 transcript and promoter activity, but not mRNA stability. Distinctly, knock-down of CRM1 had no effect on COX-2 expression by IL-1beta. Moreover, LMB did not affect IL-1beta-induced phosphorylation of ERK-1/2, JNK- 1/2, and p38 MAPK or AP-1 promoter activity. In contrast, LMB blocked IL-1beta- mediated cytosolic IkappaB-alpha degradation, p65 NF-kappaB nuclear translocation, and NF-kappaB promoter activity. CONCLUSION: LMB potently down-regulates IL-1beta- induced COX-2 at transcriptional level in A549 cells, in part, through modulation of the IkappaB-alpha/NF-kappaB pathway but independent of CRM1, MAPKs and AP-1.
Active Transport, Cell Nucleus ; Blotting, Western ; Cell Line ; Cytosol ; Down-Regulation* ; Humans ; Luciferases ; Lung Diseases ; Lung Neoplasms* ; Lung* ; NF-kappa B ; p38 Mitogen-Activated Protein Kinases ; Phosphorylation ; Prostaglandins ; RNA Stability ; RNA, Messenger ; RNA, Small Interfering ; Streptomyces ; Transcription Factor AP-1

BACKGROUND: Pregabalin is an anticonvulsant and analgesic agent that interacts selectively with the voltage-sensitive-Ca(2+)-channel alpha-2-delta subunit. The aim of this study was to evaluate whether the analgesic action of intrathecal (IT) pregabalin is associated with KATP channels in the rat formalin test. METHODS: IT PE-10 catheters were implanted in male Sprague-Dawley rats (250-300 g) under inhalation anesthesia using enflurane. Nociceptive behavior was defined as the number of hind paw flinches during 60 min after formalin injection. Ten min before formalin injection, IT drug treatments were divided into 3 groups: normal saline (NS) 20 microl (CON group); pregabalin 0.3, 1, 3 and 10 microg in NS 10 microl (PGB group); glibenclamide 100 microg in DMSO 5 microl with pregabalin 0.3, 1, 3 and 10 microg in NS 5 microl (GBC group). All the drugs were flushed with NS 10 microl. Immunohistochemistry for the KATP channel was done with a different set of rats divided into naive, NS and PGB groups. RESULTS: IT pregabalin dose-dependently decreased the flinching number only in phase 2 of formalin test. The log dose response curve of the GBC group shifted to the right with respect to that of the PGB group. Immunohistochemistry for the KATP channel expression on the spinal cord dorsal horn showed no difference among the groups 1 hr after the formalin test. CONCLUSIONS: The antinociceptive effect of pregabalin in the rat formalin test was associated with the activation of the KATP channel. However, pregabalin did not induce KATP channel expression in the spinal cord dorsal horn.
Anesthesia, Inhalation ; Animals ; Catheters ; Dimethyl Sulfoxide ; Enflurane ; Formaldehyde ; gamma-Aminobutyric Acid ; Glyburide ; Horns ; Humans ; Immunohistochemistry ; KATP Channels ; Male ; Pain Measurement ; Prostaglandins B ; Rats ; Rats, Sprague-Dawley ; Spinal Cord ; Thienamycins ; Pregabalin