Compressive strength and hydration with age of cement pastes containing finely ground sand

The aim of this work is to study the possibility of using finely ground sand as a part mass addition to Portland cement. Searching the effect of addition ground sand on development of compressive strength and hydration with age of cement pastes as a function of the percentage of ground sand ( physico-chemical and chemical effect) and the fineness ( physical effect). In order to understand better the pozzolanic effect of finely ground sand (quartz), we followed the mixtures hydration (90% OPC + 10% ground sand) by X-ray diffraction. The results proved the pozzolanic reactivity of ground sand: the main reaction is the fixation of the lime coming from the cement hydration in the presence of finely ground sand, to form calcium silicate hydrate C-S-H. Moreover, finely ground sand has an optimum effect on compressive strengths when the percentage is about 10% and a 20 µm fineness. Finely ground sand, despite its crystalline structure, presents a pozzolanic reactivity. Key words: Portland cement, finely ground sand, pozzolanic effect, hydration

A Novel Mouse c-fos Intronic Promoter That Responds to CREB and AP-1 Is Developmentally Regulated In Vivo

BACKGROUND: The c-fos proto-oncogene is an archetype for rapid and integrative transcriptional activation. Innumerable studies have focused on the canonical promoter, located upstream from the transcriptional start site. However, several regulatory sequences have been found in the first intron. METHODOLOGY/PRINCIPAL FINDINGS: Here we describe an extremely conserved region in c-fos first intron that contains a putative TATA box, and functional TRE and CRE sites. This fragment drives reporter gene activation in fibroblasts, which is enhanced by increasing intracellular calcium and cAMP and by cotransfection of CREB or c-Fos/c-Jun expression vectors. We produced transgenic mice expressing a lacZ reporter controlled by the intronic promoter. Lac Z expression of this promoter is restricted to the developing central nervous system (CNS) and the mesenchyme of developing mammary buds in embryos 12.5 days post-conception, and to brain tissue in adults. RT-QPCR analysis of tissue mRNA, including the anlage of the mammary gland and the CNS, confirms the existence of a novel, nested mRNA initiated in the first intron. CONCLUSIONS/SIGNIFICANCE: Our results provide evidence for a novel, developmentally regulated promoter in the first intron of the c-fos gene

Dynamic histone H3 methylation during gene induction: HYPB/Setd2 mediates all H3K36 trimethylation

Understanding the function of histone modifications across inducible genes in mammalian cells requires quantitative, comparative analysis of their fate during gene activation and identification of enzymes responsible. We produced high-resolution comparative maps of the distribution and dynamics of H3K4me3, H3K36me3, H3K79me2 and H3K9ac across c-fos and c-jun upon gene induction in murine fibroblasts. In unstimulated cells, continuous turnover of H3K9 acetylation occurs on all K4-trimethylated histone H3 tails; distribution of both modifications coincides across promoter and 5′ part of the coding region. In contrast, K36- and K79-methylated H3 tails, which are not dynamically acetylated, are restricted to the coding regions of these genes. Upon stimulation, transcription-dependent increases in H3K4 and H3K36 trimethylation are seen across coding regions, peaking at 5′ and 3′ ends, respectively. Addressing molecular mechanisms involved, we find that Huntingtin-interacting protein HYPB/Setd2 is responsible for virtually all global and transcription-dependent H3K36 trimethylation, but not H3K36-mono- or dimethylation, in these cells. These studies reveal four distinct layers of histone modification across inducible mammalian genes and show that HYPB/Setd2 is responsible for H3K36 trimethylation throughout the mouse nucleus

Rasd1 Modulates the Coactivator Function of NonO in the Cyclic AMP Pathway

All living organisms exhibit autonomous daily physiological and behavioural rhythms to help them synchronize with the environment. Entrainment of circadian rhythm is achieved via activation of cyclic AMP (cAMP) and mitogen-activated protein kinase signaling pathways. NonO (p54nrb) is a multifunctional protein involved in transcriptional activation of the cAMP pathway and is involved in circadian rhythm control. Rasd1 is a monomeric G protein implicated to play a pivotal role in potentiating both photic and nonphotic responses of the circadian rhythm. In this study, we have identified and validated NonO as an interacting partner of Rasd1 via affinity pulldown, co-immunoprecipitation and indirect immunofluorescence studies. The GTP-hydrolysis activity of Rasd1 is required for the functional interaction. Functional interaction of Rasd1-NonO in the cAMP pathway was investigated via reporter gene assays, chromatin immunoprecipitation and gene knockdown. We showed that Rasd1 and NonO interact at the CRE-site of specific target genes. These findings reveal a novel mechanism by which the coregulator activity of NonO can be modulated

Identification of Interferon-β-Stimulated Genes that Inhibit Angiogenesis In Vitro

Interferons (IFNs) have proven antitumor activity against a variety of human malignancies, which may result, at least in part, from inhibition of angiogenesis. The objective of this study was to identify IFN-stimulated genes (ISGs) that played a role in mediation of angiogenic inhibition. IFN-beta was a more potent antiangiogenic agent compared to IFN-alpha2b (80% versus 20%, respectively) and suggests that IFNs inhibited angiogenesis by preventing endothelial cell differentiation, and not by direct antiproliferative effects. To identify ISGs that were key inhibitors of angiogenesis, we utilized an in vitro fibrin gel angiogenic assay which closely recapitulated the in vivo processes of angiogenesis. DNA microarray analysis of IFN-beta-treated endothelial cells in the fibrin gel assay identified 11 ISGs that were induced \u3e10-fold during angiogenesis inhibition. Recombinant IP-10 inhibited angiogenesis in a dose-dependent fashion, but was a less effective inhibitor compared to IFN-beta, suggesting that additional ISGs are involved in inhibiting angiogenesis. ISG20 was upregulated by microarray analysis, but did not inhibit angiogenesis when overexpressed in human umbilical vein endothelial cells (HUVECs). However, a dominant negative mutant of ISG20 inhibited angiogenesis by 43%. Results suggest that IFN-induced angiogenic inhibition was likely mediated by multiple ISGs; our novel finding is that decreased exonuclease activity in HUVECs associated with expression of the ISG20 ExoII mutant inhibited angiogenesis

Identification of interferon-beta-stimulated genes that inhibit angiogenesis in vitro.

International audienceInterferons (IFNs) have proven antitumor activity against a variety of human malignancies, which may result, at least in part, from inhibition of angiogenesis. The objective of this study was to identify IFN-stimulated genes (ISGs) that played a role in mediation of angiogenic inhibition. IFN-beta was a more potent antiangiogenic agent compared to IFN-alpha2b (80% versus 20%, respectively) and suggests that IFNs inhibited angiogenesis by preventing endothelial cell differentiation, and not by direct antiproliferative effects. To identify ISGs that were key inhibitors of angiogenesis, we utilized an in vitro fibrin gel angiogenic assay which closely recapitulated the in vivo processes of angiogenesis. DNA microarray analysis of IFN-beta-treated endothelial cells in the fibrin gel assay identified 11 ISGs that were induced >10-fold during angiogenesis inhibition. Recombinant IP-10 inhibited angiogenesis in a dose-dependent fashion, but was a less effective inhibitor compared to IFN-beta, suggesting that additional ISGs are involved in inhibiting angiogenesis. ISG20 was upregulated by microarray analysis, but did not inhibit angiogenesis when overexpressed in human umbilical vein endothelial cells (HUVECs). However, a dominant negative mutant of ISG20 inhibited angiogenesis by 43%. Results suggest that IFN-induced angiogenic inhibition was likely mediated by multiple ISGs; our novel finding is that decreased exonuclease activity in HUVECs associated with expression of the ISG20 ExoII mutant inhibited angiogenesis