Post-Installed Metal Anchors Behavior In Cyclically Cracked Concrete

The mechanical behavior of post - installed metal anchors is well known under quasi - static loads but is mostly unknown in seismic loading conditions. Particularly, the loadbearing capacity of such construction products is greatly influenced by the presence of cracksin concrete, especially when the anchor is fixed along a crack.In seismic conditions, fasteners are expected to transfer cyclic actions as reliably aspossible, from the fixture to the concrete. At the same time, the cracks system of the concrete structure will be subjected to a variation of their width.Actually, post -installed metal anchors are covered by two codes in Europe: ETAG - 001 Guideline 6 and Eurocode 2.2 These codes require anchors testing in cracked concrete with static crack opening of 0,3 mm. A Working Group EOTA, involving a number of writers, iscurrently working on a revised version of ETAG - 001 Guideline 6 covering the seismic behavior too.Today, the only one code that cover the seismic behavior of these products is ACI 3551 which provides an experimental test with cyclic loading applied to the anchor installed in anopened crack having constant width.In this paper the results of a recent experimental test on a torque -controlled expansion anchors (bolt - type) installed in cracked concrete specimens are presented. The originality ofthese tests is that the anchors are installed along a concrete crack, which undergoes to opening and closing cycles, while the design axial load is applied to the anchor and remains constant during the test. This approach could be interpreted as complementary to the one followed by ACI 3551 code.The testing apparatus allows the monitoring of the anchor slip during theopening/closing crack cycles. Furthermore, the effects of increasing damage in the concrete and in the anchor on the residual pull - out capacity of the anchors could be estimated

SEISMIC VULNERABILITY ASSESSMENT OF A MILITARY DRY DOCK IN MESSINA

The paper summarizes the studies conducted on the military dry dock in the Port of Messina (built in 1861), to assess the seismic vulnerability. For this work was conducted an accurate research on the historical sources of Technical Office of the Italian Civil Engineers, to know the construction methods, the operations made after the earthquake of 1908 and to increase the size on 1950. Studies have included the implementation of a finite element model for seismic analysis and with a simulation of construction stages. The analysis results are evaluated against mandatory italian design code to assess the seismic vulnerability of the structure

CCAAT/enhancer-binding proteins are key regulators of human type two deiodinase expression in a placenta cell line

An appropriate concentration of intracellular T(3) is a critical determinant of placenta development and function and is mainly controlled by the activity of type II deiodinase (D2). The levels of this enzyme are finely regulated in different tissues by coordinated transcriptional mechanisms, which rely on dedicated promoter sequences (e.g. cAMP response element and TATA elements) that impart inducibility and tissue specificity to Dio2 mRNA expression. Here we show that CCAAT enhancer-binding proteins α and β (C/EBPα and C/EBPβ) promote Dio2 expression in the trophoblastic cell line JEG3 through a conserved CCAAT element, which is a novel key component of the Dio2 promoter code that confers tissue-specific expression of D2 in these cells. Increased C/EBPs levels potently induce Dio2 transcription, whereas their ablation results in loss of Dio2 mRNA. By measuring the activity of several deletion and point mutant promoter constructs, we have identified the functional CCAAT element responsible for this effect, which is located in close proximity to the most 5' TATA box. Notably, this newly identified sequence is highly conserved throughout the species and binds in vivo and in vitro C/EBP, indicating the relevance of this regulatory mechanism. Together, our results unveil a novel mechanism of regulation of D2 expression in a trophoblastic cell line, which may play a relevant role during placenta development

Antagonism of the prokineticin system prevents and reverses allodynia and inflammation in a mouse model of diabetes

Neuropathic pain is a severe diabetes complication and its treatment is not satisfactory. It is associated with neuroinflammation-related events that participate in pain generation and chronicization. Prokineticins are a new family of chemokines that has emerged as critical players in immune system, inflammation and pain. We investigated the role of prokineticins and their receptors as modulators of neuropathic pain and inflammatory responses in experimental diabetes. In streptozotocin-induced-diabetes in mice, the time course expression of prokineticin and its receptors was evaluated in spinal cord and sciatic nerves, and correlated with mechanical allodynia. Spinal cord and sciatic nerve pro- and anti-inflammatory cytokines were measured as protein and mRNA, and spinal cord GluR subunits expression studied. The effect of preventive and therapeutic treatment with the prokineticin receptor antagonist PC1 on behavioural and biochemical parameters was evaluated. Peripheral immune activation was assessed measuring macrophage and T-helper cytokine production. An up-regulation of the Prokineticin system was present in spinal cord and nerves of diabetic mice, and correlated with allodynia. Therapeutic PC1 reversed allodynia while preventive treatment blocked its development. PC1 normalized prokineticin levels and prevented the up-regulation of GluN2B subunits in the spinal cord. The antagonist restored the pro-/anti-inflammatory cytokine balance altered in spinal cord and nerves and also reduced peripheral immune system activation in diabetic mice, decreasing macrophage proinflammatory cytokines and the T-helper 1 phenotype. The prokineticin system contributes to altered sensitivity in diabetic neuropathy and its inhibition blocked both allodynia and inflammatory events underlying disease

Triple-Cut Computer-Aided Design-Computer-Aided Modeling: More Oncologic Safety Added to Precise Mandible Modeling

PURPOSE: Computer-aided design-computer-aided modeling (CAD-CAM) has become standard in mandibular reconstruction because it offers better outcomes. Occasionally, the reconstructive plans need to be changed intraoperatively and the custom-made prefabricated devices may become inadequate. We present an efficient adjunct to the standard CAD-CAM technique that resolves this problem. MATERIALS AND METHODS: Customized surgical devices with our "triple-cut" concept were used in 5 patients for mandibular reconstruction with free fibula flap (4 after mandibular resection for squamous cell carcinoma and 1 after mandibular osteoradionecrosis). In all patients the mandibular and fibular cutting guides were provided with 3 different cutting levels per side. RESULTS: Three different cutting levels on the mandible permitted an accurate resection based on the intraoperative needs. The corresponding 3 "cutting levels" on the fibula created perfectly matching segments of vascularized bone. Good contact of bony segments was obtained in all patients. CONCLUSIONS: The prefabricated triple-cut cutting guides make changing the dimensions of bony resection, while still using the prefabricated CAD-CAM reconstructive plate, possible

ESR2 Drives Mesenchymal-to-Epithelial Transition in Triple-Negative Breast Cancer and Tumorigenesis In Vivo

Estrogen receptors (ERs) have pivotal roles in the development and progression of triple-negative breast cancer (TNBC). Interactions among cancer cells and tumor microenvironment are orchestrated by the extracellular matrix that is rapidly emerging as prominent contributor of fundamental processes of breast cancer progression. Early studies have correlated ER beta expression in tumor sites with a more aggressive clinical outcome, however ER beta exact role in the progression of TNBC remains to be elucidated. Herein, we introduce the functional role of ER beta suppression following isolation of monoclonal cell populations of MDA-MB-231 breast cancer cells transfected with shRNA against human ESR2 that permanently resulted in 90% reduction of ER beta mRNA and protein levels. Further, we demonstrate that clone selection results in strongly reduced levels of the aggressive functional properties of MDA-MB-231 cells, by transforming their morphological characteristics, eliminating the mesenchymal-like traits of triple-negative breast cancer cells. Monoclonal populations of shER beta MDA-MB-231 cells undergo universal matrix reorganization and pass on a mesenchymal-to-epithelial transition state. These striking changes are encompassed by the total prevention of tumorigenesis in vivo following ER beta maximum suppression and isolation of monoclonal cell populations in TNBC cells. We propose that these novel findings highlight the promising role of ER beta targeting in future pharmaceutical approaches for managing the metastatic dynamics of TNBC breast cancer

The airplane crash at the "Pirelli" tall building

This paper is meant to deliver an overview on the damages and the following repairs of the structures of the 26th and 27th floor due to the airplane accident occurred on April, the 18th 2002. An aircraft 112 TC Commander impacted the facade of the Pirelli skyscraper getting into the building, where its gasoline tanks exploded. The first part of the paper focuses on a simplified analysis with the aims of evaluating the blast impulse and the peak pressure caused by the explosion on the floors structures. Then, a description of the realignment of the deck and the repairing operations are briefly summarized

The prokineticin receptor agonist Bv8 decreases IL-10 and IL-4 production in mice splenocytes by activating prokineticin receptor-1

<p>Abstract</p> <p>Background</p> <p>Bv8, prokineticin-1, or endocrine gland-vascular endothelial growth factor, and prokineticin-2 are recently isolated peptide agonists of two G protein-coupled receptors, prokineticin receptor-1 (PROKR 1) and PROKR 2, and have been described as affecting a number of myeloid cell functions. We evaluated the impact of Bv8 on lymphoid cells by investigating its ability to modulate T cell cytokine balance in mouse.</p> <p>Results</p> <p>The production of T-helper1 cytokines (IL-2, IFN-γ and IL-1β), the T-helper 2 cytokine IL-4, and the anti-inflammatory cytokine IL-10 by mouse splenocytes was evaluated after polyclonal stimulation or immunisation with the keyhole limpet hemocyanin protein antigen by measuring cytokine levels. When added <it>in vitro </it>to Con-A-stimulated splenocytes, Bv8 significantly increased IL-1β and decreased IL-4 and IL-10; IL-2 and IFN-γ were not affected. Similar results were obtained when Bv8 was administered <it>in vivo</it>. In KLH-immunised mice, splenocytes restimulated <it>in vitro </it>with KLH and Bv8 produced significantly smaller amounts of IL-4 and IL-10. KLH-induced IL-10 and IL-4 production was also significantly blunted in animals administered Bv8 <it>in vivo </it>at the time of KLH immunisation or two weeks later. The Bv8-induced effects were lost in mice lacking the PROKR 1 gene, thus indicating that PROKR 1 is the receptor involved in the modulation of cytokines.</p> <p>Conclusion</p> <p>These findings indicate that Bv8/prokineticin-1 is a novel modulator of lymphoid functions, and may be a suitable target for new immunopharmacological strategies.</p