NPY Y1 and VPAC1 receptor expression in human dental pulps

Neuropeptides such as neuropeptide Y (NPY) and vasoactive intestinal polypeptide (VIP) have been shown by our research group to be present in human dental pulp tissue. Neuropeptides cannot cross cell membranes and therefore to exert their biological effects they must bind to selected receptors on the surface of target cell membranes. However, the expression of receptor proteins for NPY and/or VIP have yet to be reported in human pulp tissue. The presence of neuropeptide receptors can be conveniently determined by Western blotting using specific anti-receptor antibodies. Objectives: The aim of this work was to identify the presence of the NPY Y1 receptor and the VIP receptor VPAC1 in human dental pulp tissue from both intact and carious teeth using Western blotting. Methods: Pulp tissue was collected from both intact and carious teeth and membrane preparations from these tissues were then subject to sodium dodecyl sulphate gel electrophoresis (SDS-PAGE), transferred to nitrocellulose and probed with specific antibodies to either the NPY Y1 receptor or the VPAC1 receptor. Results: Individual Western blotting experiments revealed the presence of immunoreactive bands corresponding to the known molecular weights of the NPY Y1 and VPAC1 receptor proteins in both intact and carious pulp samples. Conclusions: Demonstration of the presence of NPY Y1 and VPAC1 receptor protein expression in pulpal tissue from intact and carious teeth provides further support for the roles of these neuropeptides in pulpal health and disease.

S.C. Dept. of Natural Resources Annual Accountability Report 1994/95

Each year the South Carolina Department of Natural Resources reports to the Office of State Budget that includes the agency's mission, goals and objectives to accomplish the mission, and performance measures regarding the goals and objectives.

Replica management in real-time Ada 95 applications

In this paper, we present some of the fault tolerance management mechanisms being implemented in the Multi-μ architecture, namely its support for replica non-determinism. In this architecture, fault tolerance is achieved by node active replication, with software based replica management and fault tolerance transparent algorithms. A software layer implemented between the application and the real-time kernel, the Fault Tolerance Manager (FTManager), is the responsible for the transparent incorporation of the fault tolerance mechanisms The active replication model can be implemented either imposing replica determinism or keeping replica consistency at critical points, by means of interactive agreement mechanisms. One of the Multi-μ architecture goals is to identify such critical points, relieving the underlying system from performing the interactive agreement in every Ada dispatching point.

Multi-μ: an Ada 95 based architecture for fault tolerance support of real-time systems

This paper presents an architecture (Multi-μ) being implemented to study and develop software based fault tolerant mechanisms for Real-Time Systems, using the Ada language (Ada 95) and Commercial Off-The-Shelf (COTS) components. Several issues regarding fault tolerance are presented and mechanisms to achieve fault tolerance by software active replication in Ada 95 are discussed. The Multi-μ architecture, based on a specifically proposed Fault Tolerance Manager (FTManager), is then described. Finally, some considerations are made about the work being done and essential future developments.

Y1 receptor knockout increases nociception and prevents the anti-allodynic actions of NPY.

OBJECTIVE: Recent pharmacologic studies in our laboratory have suggested that the spinal neuropeptide Y (NPY) Y1 receptor contributes to pain inhibition and to the analgesic effects of NPY. To rule out off-target effects, the present study used Y1-receptor-deficient (-/-) mice to further explore the contribution of Y1 receptors to pain modulation. METHODS AND RESULTS: Y1(-/-) mice exhibited reduced latency in the hotplate test of acute pain and a longer-lasting heat allodynia in the complete Freund's adjuvant (CFA) model of inflammatory pain. Y1 deletion did not change CFA-induced inflammation. Upon targeting the spinal NPY systems with intrathecal drug delivery, NPY reduced tactile and heat allodynia in the CFA model and the partial sciatic nerve ligation model of neuropathic pain. Importantly, we show for the first time that NPY does not exert these anti-allodynic effects in Y1(-/-) mice. Furthermore, in nerve-injured CD1 mice, concomitant injection of the potent Y1 antagonist BIBO3304 prevented the anti-allodynic actions of NPY. Neither NPY nor BIBO3304 altered performance on the Rotorod test, arguing against an indirect effect of motor function. CONCLUSION: The Y1 receptor contributes to pain inhibition and to the analgesic effects of NPY.

Horace (2), Perse (95), Juvénal (150v) et Térence (163v).

On y a ajouté plusieurs pièces fugitives en prose et en vers (1), une table de comput (94v), et des règles de quantité intitulées "Serviolus" (162).

Justinianus imperator, Institutiones (2-44). - Summa Codicis (44v-95).

Le ms. a appartenu à Antoine Loisel (signature "Ant. Loisel" au f. 2), avocat et grand-père de Claude Joly, chantre de Notre-Dame qui légua les mss. dont il avait hérité de son grand-père au chapitre de Notre-Dame de Paris en 1680. Sur le f. 1v figure l'ex-libris "A la bibliotheque de l'Eglise de Paris", suivi de la cote F11 (XVIIe s.). Notre-Dame.

Recueil de poésies, par « HENRY BAULDE » (fol. 30, 32, 35, 36, 37, 39, 40, 43, 44, 46, 47, 56, 59, 60, 61, 65, 68, 69, 70, 73, 74), « ALAIN CHARRETIER » (fol. 15), « JEHAN DAUTON » (fol. 9), « JEHAN MAROT » (fol. 29, 30), « JEHAN MOLINET » (fol. 77, 85, 90, 93, 94, 95) et « JEHAN ROBERTET » (fol. 1, 75).

Commençant par : « Estant couché soubz ung myrthe plaisant, Et maintz chasteaulx en Espaigne faisant... » et finissant par : « Sans parage ou riens n'est nect, Moulu d'un groz Moulinet. Fin de la complaincte de Grece, composée par le dict Molinet » .