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Statement of Problem. Fabrication technique, precementation, and cementation operative procedures can induce significant modification of the stressing patterns throughout the thickness of some classes of dental ceramic materials. Objectives. To estimate, by means of the deflection test, residual stress in restorative dental ceramic following fabrication technique, precementation, and resin cement coating procedures and to relate it to the elastic property of the ceramic material tested. Materials and Methods. From IPS e.max® Press, lithium disilicate heat-pressed glass-ceramic (elastic modulus of 95 ± 5 GPa) disc-shaped specimens (n = 10) were made according to the manufacturer's instructions. One surface of the specimens was polished to provide accurate baseline profilometric measurements (reference surface). Deflection measurements were performed after polishing and annealing alumina air-particle abrasion of the unpolished surface followed by resin cement coating of the alumina air-particle abraded surface. The specimens were reprofiled at 24, 48, and 168 hrs after coating. The Friedman test followed by Dunn's multiple comparison test was employed to identify significant differences (p<0.05). To compare the difference in mean of maximum mechanical deflection, after cement coating at 0 hr, between two different ceramic materials (IPS e.max Press and Vitadur Alpha (result from another study)), Student's t-test for unpaired data was performed. Results. Baseline profilometric measurements identified a convex form on the polished surface of the ceramic discs with a mean of maximum mechanical deflection of 4.45 ± 0.87 μm. A significant reduction in convexity of the polished specimens was characterized after alumina air-particle abrasion of the unpolished surface. The mean deflection significantly increased after resin cement coating and did not change over the time investigated. Conclusions. The precementation treatment, namely, alumina air-particle abrasion and cementation procedure of IPS e.max® Press glass-ceramic disc-shaped specimens generates stress that induced mechanical deformation. However, a dental ceramic material with higher elastic modulus (stiffer) would minimize stress-inducing mechanical deformation. [ABSTRACT FROM AUTHOR]

Highlights: [•] Bradykinin (BK) may play a role in the pathophysiology of epilepsy. [•] We found that B2 BK receptors are implicated in the early phase of epileptogenesis. [•] Findings implicate that B2 antagonists may be used to prevent epileptogenesis. [ABSTRACT FROM AUTHOR]

1 The modulation exerted by nociceptin/orphanin FQ (NC) on noradrenaline (NE) release in rodent cerebral cortex slices and synaptosomes was studied. 2 Rat, mouse and guinea-pig cortical slices and synaptosomes were preincubated with 0.1 micro M [(3)H]-NE and superfused. NE release was evoked by 2 min of electrical (3 Hz) stimulation in slices and by 1 min pulse of 10 mM KCl in synaptosomes. 3 In rat cortical slices, 0.01-3 micro M NC reduced the evoked [(3)H]-NE efflux (E(max)-54%), with a bell-shaped concentration-response curve, which regained its monotonic nature in the presence of either 0.1 micro M naloxone (NX) or 30 micro M bicuculline. In synaptosomes, the NC effect curve was sygmoidal in shape and reached a plateau at 1 micro M concentration. 4 In the rat, both 1 micro M [Phe(1)psi(CH(2)-NH)Gly(2)]NC(1-13)NH(2) and 10 micro M [Nphe(1)]NC(1-13)NH(2) (NPhe) antagonised NC-induced inhibition, without per se modifying [(3)H]-NE efflux. The effects of 0.3-1 micro M NC concentrations were partially prevented by 1 micro M NX; 1 micro M D-Phe-Cys-Thr-D-Trp-Orn-Thr-Pen-Thr-NH(2) (CTOP) was also an effective antagonist, but 0.1 micro M norbinaltorphimine was not. 5 In the mouse cerebral cortex, NC-induced inhibition of NE release (pEC(50) 6.87, E(max)-61%, in the slices) was prevented by Nphe but was NX-insensitive. In guinea-pig cortical slices, NC effect (pEC(50) 6.22, E(max)-38%) was prevented by Nphe, but was NX-insensitive. 6 These findings demonstrate that NC inhibits NE release from rodent cerebral cortex via presynaptically located ORL(1) receptors. In the rat, micro opioid and GABA(A) receptors are involved as well. [ABSTRACT FROM AUTHOR]

Abstract: A link between temporal lobe epilepsy (the most common epileptic syndrome in adults) and neuropeptides has been established. Among neuropeptides, the possible involvement of bradykinin has recently received attention. An autoradiographic analysis has shown that B1 receptors, which are physiologically absent, are expressed at high levels in the rat brain after completion of kindling, a model of temporal lobe epilepsy. Thus, the present work aimed at investigating the functional implications of this observation, by studying the effect of B1 receptor activation on extracellular glutamate levels in the kindled hippocampus. Microdialysis experiments have been performed in two groups of rats, control and kindled. Glutamate outflow has been measured under basal conditions and after chemical stimulation with high K+ (100mM in the dialysis solution). Basal glutamate outflow in kindled animals was significantly higher than in controls. High K+-evoked glutamate outflow was also more pronounced in kindled animals, consistent with the latent hyperexcitability of the epileptic tissue. The B1 receptor agonist Lys-des-Arg9-BK induced an increase of basal and high K+-evoked glutamate outflow in kindled but not in control rats, and the selective B1 receptor antagonist R-715 prevented both these effects. Furthermore, R-715 significantly reduced high K+-evoked glutamate outflow when applied alone. These data suggest that the bradykinin system contributes to the modulation of epileptic neuronal excitability through B1 receptors. [Copyright &y& Elsevier]

Summary: Purpose: To analyze whether the subcellular localization of the messenger RNAs (mRNAs) coding for the neurotrophin brain-derived neurotrophic factor (BDNF), its receptor TrkB, and the α and β subunits of calcium-calmodulin–dependent kinase II (CaMKII) are modified after pilocarpine and kindled seizures. Methods: Epilepsy models: pilocarpine and kindling. Analysis of mRNA levels in the dendrites: high-resolution, nonradioactive in situ hybridization. Results: Nonstimulated rats: BDNF, TrkB, and CaMKII-β mRNAs localized in the soma and in the proximal dendrites of hippocampal pyramidal cells, and in the soma only of dentate gyrus (DG) granule cells; CaMKII-α mRNA localized throughout the dendritic length in neurons of all hippocampal subfields. Pilocarpine seizures: increased staining levels of CaMKII-α mRNA throughout the whole dendritic length in all hippocampal subfields; induction of CaMKII-β, BDNF, and TrkB mRNAs dendritic targeting in CA1, CA3, and DG neurons. Class 2 kindled seizures: increase in dendritic staining intensity for CaMKII-α in CA1, CA3, and DG neurons; induction of dendritic localization of CaMKII-β, BDNF, and TrkB mRNAs in CA3 neurons. Fully kindled seizures: no change in the subcellular distribution of BDNF, TrkB and CaMKII-β mRNAs; reduction of CaMKII-α mRNA dendritic staining, as compared with unstimulated kindled animals. Conclusions: Data provide evidence that BDNF, TrkB, and CaMKII-α and -β mRNAs are accumulated in the dendrites of specific hippocampal neurons during pilocarpine seizures and kindling development. The dendritic targeting of these genes may be causally involved in epileptogenesis and thus may represent a new therapeutic target for some forms of partial epilepsy. [ABSTRACT FROM AUTHOR]