Salivary alpha amylase and cortisol levels in children with global developmental delay and their relation with the expectation of dental care and behavior during the intervention

The purpose of this study was to analyze the alpha-amylase (sAA) and cortisol levels in children with Global developmental delay (GDD) before and after dental treatment and its association with the children's behavior during treatment. The morning salivary cortisol levels and activity of sAA of 33 children with GDD were evaluated before and after dental treatment and were compared to 19 healthy children. The behavior of children with GDD during dental care was assessed by the Frankl scale. Children with GDD showed lower levels of sAA activity than healthy children, but this result was not significant. The salivary cortisol levels were similar between GOD and healthy children. GDD children showed increased levels of sAA (but not cortisol) prior to the dental treatment as compared to the post-treatment phase. GOD children who showed less favorable behavior during dental care had higher levels of sAA and salivary cortisol than GOD children with more favorable behavior, but only the sAA results were significant. In conclusion, GOD children show hyperactivity of the SNS-axis in anticipation of dental treatment which indicates the need for strategies to reduce their anxiety levels before and during dental care. (C) 2011 Elsevier Ltd. All rights reserved.

NaF treatment increases TNF-alpha and resistin concentrations and reduces insulin signal in rats

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Expression of interferon-gamma, interferon-alpha and related genes in individuals with Down syndrome and periodontitis

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

MKK3/6-p38 MAPK signaling is required for IL-1 beta and TNF-alpha-induced RANKL expression in bone marrow stromal cells

Coupled bone turnover is directed by the expression of receptor-activated NF-kappa B ligand (RANKL) and its decoy receptor, osteoprotegerin (OPG). Proinflammatory cytokines, such as interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) induce RANKL expression in bone marrow stromal cells. Here, we report that IL-1 beta and TNF-alpha-induced RANKL requires p38 mitogen-activating protein kinase (MAPK) pathway activation for maximal expression. Real-time PCR was used to assess the p38 contribution toward IL-1 beta and TNF-alpha-induced RANKL mRNA expression. Steady-state RANKL RNA levels were increased approximately 17-fold by IL-1 beta treatment and subsequently reduced similar to 70%-90% when p38 MAPK was inhibited with SB203580. RANKL mRNA stability data indicated that p38 MAPK did not alter the rate of mRNA decay in IL-1 beta-induced cells. Using a RANKL-luciferase cell line receptor containing a 120-kB segment of the 5' flanking region of the RANKL gene, reporter expression was stimulated 4-5-fold by IL-1 beta or TNF-alpha treatment. IL-1 beta-induced RANKL reporter expression was completely blocked with specific p38 inhibitors as well as dominant negative mutant constructs of MAPK kinase-3 and -6. In addition, blocking p38 signaling in bone marrow stromal cells partially inhibited IL-1 beta and TNF-alpha-induced osteoclastogenesis in vitro. Results from these studies indicate that p38 MAPK is a major signaling pathway involved in IL-1 beta and TNF-alpha-induced RANKL expression in bone marrow stromal cells.

Antigenic Activity of Bacterial Endodontic Contents from Primary Root Canal Infection with Periapical Lesions against Macrophage in the Release of Interleukin-1 beta and Tumor Necrosis Factor alpha

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Tumor Necrosis Factor alpha and Interleukin-1 beta Modulate Calcium and Nitric Oxide Signaling in Mechanically Stimulated Osteocytes

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Involvement of forebrain imidazoline and alpha(2)-adrenergic receptors in the antidipsogenic response to moxonidine

We investigated the participation of central alpha(2)-adrenoceptors and imidazoline receptors in the inhibition of water deprivation-induced water intake in rats. The alpha(2)-adrenoceptor and imidazoline antagonist idazoxan (320 nmol), but not the alpha(2)-adrenoceptor antagonist yohimbine, abolished the antidipsogenic effect of moxonidine (alpha(2)-adrenoceptor and imidazoline agonist, 20 nmol) microinjected into the medial septal area. Yohimbine abolished the antidipsogenic effect of moxonidine intracerebroventricularly. Therefore, central moxonidine may inhibit water intake acting independently on both imidazoline receptors and alpha(2)-adrenoceptors at different forebrain sites.