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Hox genes encode Homeodomain-containing transcription factors, which specify segmental identities along the anterior-posterior axis. Functional changes in Hox genes have been directly implicated in the evolution of body plans across the metazoan lineage. The Hox protein Ultrabithorax (Ubx) is expressed and required in developing third thoracic (T3) segments in holometabolous insects studied so far, particularly, of the order Coleoptera, Lepidoptera and Diptera. Ubx function is key to specify differential development of the second (T2) and T3 thoracic segments in these insects. While Ubx is expressed in the third thoracic segment in developing larvae of Hymenopteran Apis mellifera, the morphological differences between T2 and T3 are subtle. To identify evolutionary changes that are behind the differential function of Ubx in these two insects, which are diverged for more than 350 million years, we performed comparative analyses of genome wide Ubx-binding sites between Drosophila and Apis. Our studies reveal that a motif with a TAAAT core is a preferred binding site for Ubx in Drosophila, but not in Apis. Biochemical and transgenic assays suggest that in Drosophila, TAAAT core sequence in the Ubx binding sites is required for Ubx-mediated regulation of two of its target genes studied here. CG13222, a gene that is normally upregulated by Ubx and vestigial (vg), whose expression is repressed by Ubx in T3. Interestingly, changing the TAAT site to a TAAAT site was sufficient to bring an otherwise unresponsive enhancer of the vg gene from Apis under the control of Ubx in a Drosophila transgenic assay. Taken together, our results suggest an evolutionary mechanism by which critical wing patterning genes might have come under the regulation of Ubx in the Dipteran lineage.

For temperatures above 750°C, TiAl alloys still show insufficient oxidation resistance and suffer from environmental embrittlement. This work focuses on the surface modification of alloys and development of coatings against environmental embrittlement, as well as on testing of mechanical properties after high temperature oxidation. Aluminum enriched coatings (between 50 and 60 at.%) containing alloying elements, i.e. Cr, Nb, Si, Y, to improve the oxidation behavior and the corrosion resistance have been produced by MO-CVD, CVD, PVD and thermal spraying techniques (HVOF, APS), and have subsequently been chemically modified with halogen elements, notably fluorine. The mechanical properties have been studied by means of 4-point bending and tensile tests on coated samples after 100h oxidation at 900 °C in laboratory air. The CVD process combined with fluorine treatment using plasma immersion implantation (PI³) of F offers the best combination to remedy environmental embrittlement. It has been shown in particular that 90% of the initial fracture strain and fracture stress can be maintained.

Due to their excellent density-specific properties, titanium aluminide (TiAl) alloys have been identified as high-payoff materials for advanced aerospace and power generation applications in the medium-temperature (600°-750°C) range. They have recently been applied as structural materials for turbine blades in the low-pressure section of the GEnx jet engine. These alloys, however, are prone to both oxidation and embrittlement when exposed to oxidizing environments at temperatures above ~ 750°C. Under such conditions, TiAl alloys form a mixed (TiO2+Al2O3) non-protective oxide scale resulting from the difference in both the growth kinetics of the two oxides, and the chemical activity of the constituent elements, Ti and Al. Thus, for high-temperature (> 750°C) applications, an oxidation protection coating is needed to prevent environmental damage of the base alloy without degrading its initial mechanical properties. The present work has focused on the development of coatings for the efficient oxidation protection of TiAl alloys at high temperatures. Aluminum-rich TiAl coatings (50 to 60 at.%Al) have been produced by either chemical vapor deposition (MO-CVD), physical vapor deposition (PVD) or thermal spraying (HVOF, APS) techniques onto a GE alloy (Ti-48Al-2Cr-2Nb) qualified for aerospace applications. The coating surface has then been modified by plasma immersion ion implantation (PIII) of fluorine to promote the formation of a protective alumina-containing scale relying on the so-called halogen effect. For the PIII processing, either difluoromethane and argon (CH2F2/Ar) or silicon tetrafluoride and argon (SiF4/Ar) has been used as the F-containing precursor gas. The resulting F-implanted coatings have been exposed to oxidative/corrosive environments at 850°C for 350 h, and have shown a high degree of oxidation resistance. The mechanical properties of the coated samples have been examined by 4-point bend, tensile and fatigue testing after oxidation in laboratory air at 900°C for 100 h. Combining a CVD process with PIII of F (the CH2F2/Ar process) has been found to give the best results in terms of efficient environmental protection against oxidation and embrittlement. It has also been established that more than 90% of the initial mechanical properties of the substrate TiAl alloy can be retained after the application of such a protective coating.

We have previously shown that PKD1, the gene encoding Polycystin-1 (or TRPP1) is expressed in human odontoblasts and that this protein is localized at the primary cilium of the cell. Nevertheless, its function remain unclear in this cell even if studies on osteoblasts, osteocytes and chondrocytes give TRPP1 as a promising candidate for mechanotransduction in response to mechanical stress. Consequently, to evaluate the role of TRPP1 in this transduction process, we needed first to generate an in vitro murine model down expressing Pkd1. Using lentivirus-mediated shRNA technology, we obtained a 60% suppression of Pkd1 mRNA expression in transfected MO6-G3 cells associated with a decrease of cell proliferation. Thus, establishment of this murine odontoblast model underexpressing Pkd1 associated with applied mechanical forces (compression or shear stress) will allow us to go further in the determination of TRPP1 involvement in odontoblasts mechanotransduction. Nous avons montré précédemment que PKD1, le gène codant pour la polycystine 1 ou TRPP1, est exprimé dans les cultures d’odontoblastes humains avec une localisation préférentielle de la protéine au niveau des cils primaires. Cependant, la fonction de TRPP1 reste à ce jour inconnue malgré un rôle potentiel de mécanotransducteur mis en évidence dans les ostéoblastes, ostéocytes et chondrocytes. Pour évaluer le rôle de cette protéine dans les odontoblastes nous avons choisi de mettre au point un modèle cellulaire sous-exprimant Pkd1. Ainsi, à l’aide de shRNA, nous avons obtenu une lignée cellulaire de souris (MO6-G3) sous-exprimant de façon stable Pkd1 (60% de sous-expression), et présentant une diminution de la prolifération cellulaire. Ce nouveau modèle cellulaire associé à l’application de forces mécaniques (compression ou étirement) devrait nous permettre d’évaluer l’implication de TRPP1 dans les processus de mécanotransduction des odontoblastes.

Selecting the best environmentally conscious manufacturing (ECM) program alternative is an important problem in the manufacturing environment. This paper presents a combinatorial mathematics approach that considers the values of the attributes and their relative importance together to provide a better accurate evaluation of the alternatives. Also, the approach allows the decision maker to systematically assign the values of relative importance to the attributes and fuzzy logic is used for conversion of qualitative attributes into quantitative attributes. An example is included to illustrate the approach.

Human odontoblasts are neural crest-derived, dentin-producing mesenchymal cells aligned at the periphery of the dental pulp. They become exposed to cariogenic oral bacteria as these progressively demineralise enamel then dentin to gain access to the pulp. Due to their situation at the dentin-pulp interface, odontoblasts are the first cells encountered by invading pathogens and/or their released components, and represent, in the tooth, the first line of defence for the host. Previous studies have shown that odontoblasts are able to sense pathogens and elicit innate immunity. In particular, they express several pathogen recognition receptors of the Toll-like receptor (TLR) and nucleotide-binding oligomerisation domain (NOD) families, which allow them to recognize specific bacterial and viral components. So far, most studies aiming at elucidating the role of odontoblasts in the dental pulp innate response have focused on Gram-positive bacteria, as these largely dominate the carious microflora in initial and moderate dentin caries lesions. In vitro, odontoblasts were found to be sensitive to Gram-positive bacteria-derived components, mainly lipoteichoic acid which is recognized through cell membrane TLR2. Our studies have shown that engagement of odontoblast TLR2 by LTA triggers TLR2 and NOD2 up-regulation, NF-B nuclear translocation, production of various chemokines including CCL2, CXCL1, CXCL2, CXCL8 and CXCL10, while promoting immature dendritic cell recruitment. Conversely, LTA down-regulates major dentin matrix components, including collagen type I and dentin sialophosphoprotein, as well as TGF-b1, a known inducer of dentin formation. We provide here additional data showing the fine localization of NOD2 in healthy dental pulps, as well as differential regulation of TLR2, TLR4, NOD2, CCL2 and CXCL8 genes by LTA and the synthetic TLR2 agonists Pam2CSK4 and Pam3CSK4. It appears from the aforementioned data that odontoblast-triggered immune events constitute potential targets for interrupting the signaling cascades which lead to excessive immune response and necrosis in the dental pulp tissue challenged with cariogenic bacteria. In particular, preventing Gram-positive bacteria recognition or signal transduction by pattern recognition receptors may represent a valuable strategy to achieve this goal. Future studies in the field will pave the way for designing novel therapeutic agents which modulate odontoblast behaviour to promote pulp healing and repair.