Micro-Electro-Mechanical-Systems (MEMS) and Fluid Flows

The micromachining technology that emerged in the late 1980s can provide micron-sized sensors and actuators. These micro transducers are able to be integrated with signal conditioning and processing circuitry to form micro-electro-mechanical-systems (MEMS) that can perform real-time distributed control. This capability opens up a new territory for flow control research. On the other hand, surface effects dominate the fluid flowing through these miniature mechanical devices because of the large surface-to-volume ratio in micron-scale configurations. We need to reexamine the surface forces in the momentum equation. Owing to their smallness, gas flows experience large Knudsen numbers, and therefore boundary conditions need to be modified. Besides being an enabling technology, MEMS also provide many challenges for fundamental flow-science research

Crystalline silicate dust around evolved stars I. The sample stars

This is the first paper in a series of three where we present the first comprehensive inventory of solid state emission bands observed in a sample of 17 oxygen-rich circumstellar dust shells surrounding evolved stars. The data were taken with the Short and Long Wavelength Spectrographs on board of the Infrared Space Observatory (ISO) and cover the 2.4 to 195 micron wavelength range. The spectra show the presence of broad 10 and 18 micron bands that can be attributed to amorphous silicates. In addition, at least 49 narrow bands are found whose position and width indicate they can be attributed to crystalline silicates. Almost all of these bands were not known before ISO. We have measured the peak positions, widths and strengths of the individual, continuum subtracted bands. Based on these measurements, we were able to order the spectra in sequence of decreasing crystalline silicate band strength. We found that the strength of the emission bands correlates with the geometry of the circumstellar shell, as derived from direct imaging or inferred from the shape of the spectral energy distribution. This naturally divides the sample into objects that show a disk-like geometry (strong crystalline silicate bands), and objects whose dust shell is characteristic of an outflow (weak crystalline silicate bands). All stars with the 33.6 micron forsterite band stronger than 20 percent over continuum are disk sources. We define spectral regions (called complexes) where a concentration of emission bands is evident, at 10, 18, 23, 28, 33, 40 and 60 micron. We derive average shapes for these complexes and compare these to the individual band shapes of the programme stars.Comment: 41 pages, 20 figures, accepted by A&A. Tables 4 to 20 are only available in electronic form at the CDS via anonymous ftp to cdsarc.u-strasbg.fr (130.79.128.5) or via http://cdsweb.u-strasbg.fr/cgi-bin/qcat?J/A+A

Inhibition of sphingosine 1-phosphate protects mice against chondrocyte catabolism and osteoarthritis

Summary Objective Cartilage loss observed in osteoarthritis (OA) is prevented when osteoclasts in the subchondral bone are inhibited in mice. Here, we investigated the role of the osteoclast secretome and of the lipid mediator sphingosine 1-phosphate (S1P) in chondrocyte metabolism and OA. Materials and methods We used SphK1LysMCre and wild type mice to assess the effect of murine osteoclast secretome in chondrocyte metabolism. Gene and protein expressions of matrix metalloproteinase (Mmp) were quantified in chondrocytes and explants by RT-qPCR and Western blots. SphK1LysMCre mice or wild type mice treated with S1P2 receptor inhibitor JTE013 or anti-S1P neutralizing antibody sphingomab are analyzed by OA score and immunohistochemistry. Results The osteoclast secretome increased the expression of Mmp3 and Mmp13 in murine chondrocytes and cartilage explants and activated the JNK signaling pathway, which led to matrix degradation. JTE013 reversed the osteoclast-mediated chondrocyte catabolism and protected mice against OA, suggesting that osteoclastic S1P contributes to cartilage damage in OA via S1P/S1P2 signaling. The activity of sphingosine kinase 1 (SphK1) increased with osteoclast differentiation, and its expression was enhanced in subchondral bone of mice with OA. The expression of Mmp3 and Mmp13 in chondrocytes was low upon stimulation with the secretome of Sphk1-lacking osteoclasts. Cartilage damage was significantly reduced in SphK1LysMCre mice, but not the synovial inflammation. Finally, intra-articular administration of sphingomab inhibited the cartilage damage and synovial inflammation. Conclusions Lack of S1P in myeloid cells and local S1P neutralization alleviates from osteoarthritis in mice. These data identify S1P as a therapeutic target in OA.The authors thank Alexandre Garcia for measurements of S1P. The work was supported by the Sybil SP7 European project and the “Fondation de l’Avenir”. JT and SV received grants from the Deutsche Forschungsgemeinschaft within the collaborative research center SFB1149.Peer reviewe

Global modeling of tropospheric iodine aerosol

Natural aerosols play a central role in the Earth system. The conversion of dimethyl sulfide to sulfuric acid is the dominant source of oceanic secondary aerosol. Ocean emitted iodine can also produce aerosol. Using a GEOS-Chem model, we present a simulation of iodine aerosol. The simulation compares well with the limited observational data set. Iodine aerosol concentrations are highest in the tropical marine boundary layer (MBL) averaging 5.2 ng (I) m −3 with monthly maximum concentrations of 90 ng (I) m −3. These masses are small compared to sulfate (0.75% of MBL burden, up to 11% regionally) but are more significant compared to dimethyl sulfide sourced sulfate (3% of the MBL burden, up to 101% regionally). In the preindustrial, iodine aerosol makes up 0.88% of the MBL burden sulfate mass and regionally up to 21%. Iodine aerosol may be an important regional mechanism for ocean-atmosphere interaction

Upregulation of MMP-13 and TIMP-1 expression in response to mechanical strain in MC3T3-E1 osteoblastic cells

<p>Abstract</p> <p>Background</p> <p>Mechanical strain plays a significant role in the regulation of bone matrix turnover, which is mediated in part by matrix metalloproteinase (MMP)-13 and tissue inhibitors of matrix metalloproteinase (TIMP)-1. However, little is known about the correlation between mechanical strain and osteoblastic cell activities, including extracellular matrix (ECM) metabolism. Herein, we determined the effect of different magnitudes of cyclic tensile strain (0%, 6%, 12%, and 18%) on MMP-13 and TIMP-1 mRNA and protein expression in MC3T3-E1 osteoblasts. Furthermore, we employed specific inhibitors to examine the role of distinct signal transduction pathways known to mediate cellular responses to mechanical strain.</p> <p>Results</p> <p>We identified a magnitude-dependent increase in MMP-13 and TIMP-1 mRNA and protein levels in response to mechanical strains corresponding to 6%, 12%, and 18% elongation. The strain-induced increases in MMP-13 and TIMP-1 mRNA expression were inhibited by PD098059 and cycloheximide, respectively.</p> <p>Conclusions</p> <p>Our results suggest a mechanism for the regulation of bone matrix metabolism mediated by the differential expression of MMP-13 and TIMP-1 in response to increasing magnitudes of mechanical strain.</p

Mechanism of Dinitrochlorobenzene-Induced Dermatitis in Mice: Role of Specific Antibodies in Pathogenesis

Dinitrochlorobenzene-induced contact hypersensitivity is widely considered as a cell-mediated rather than antibody-mediated immune response. At present, very little is known about the role of antigen-specific antibodies and B cells in the development of dinitrochlorobenzene-induced hypersensitivity reactions, and this is the subject of the present investigation.Data obtained from multiple lines of experiments unequivocally showed that the formation of dinitrochlorobenzene-specific Abs played an important role in the development of dinitrochlorobenzene-induced contact hypersensitivity. The appearance of dinitrochlorobenzene-induced skin dermatitis matched in timing the appearance of the circulating dinitrochlorobenzene-specific antibodies. Adoptive transfer of sera containing dinitrochlorobenzene-specific antibodies from dinitrochlorobenzene-treated mice elicited a much stronger hypersensitivity reaction than the adoptive transfer of lymphocytes from the same donors. Moreover, dinitrochlorobenzene-induced contact hypersensitivity was strongly suppressed in B cell-deficient mice with no DNCB-specific antibodies. It was also observed that treatment of animals with dinitrochlorobenzene polarized Th cells into Th2 differentiation by increasing the production of Th2 cytokines while decreasing the production of Th1 cytokines.In striking contrast to the long-held belief that dinitrochlorobenzene-induced contact hypersensitivity is a cell-mediated immune response, the results of our present study demonstrated that the production of dinitrochlorobenzene-specific antibodies by activated B cells played an indispensible role in the pathogenesis of dinitrochlorobenzene-induced CHS. These findings may provide new possibilities in the treatment of human contact hypersensitivity conditions

Glucocorticoids in T cell apoptosis and function

Glucocorticoids (GCs) are a class of steroid hormones which regulate a variety of essential biological functions. The profound anti-inflammatory and immunosuppressive activity of synthetic GCs, combined with their power to induce lymphocyte apoptosis place them among the most commonly prescribed drugs worldwide. Endogenous GCs also exert a wide range of immunomodulatory activities, including the control of T cell homeostasis. Most, if not all of these effects are mediated through the glucocorticoid receptor, a member of the nuclear receptor superfamily. However, the signaling pathways and their cell type specificity remain poorly defined. In this review, we summarize our present knowledge on GC action, the mechanisms employed to induce apoptosis and the currently discussed models of how they may participate in thymocyte development. Although our knowledge in this field has substantially increased during recent years, we are still far from a comprehensive picture of the role that GCs play in T lymphocytes