367 research outputs found

    On Recognizing Transparent Objects in Domestic Environments Using Fusion of Multiple Sensor Modalities

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    Current object recognition methods fail on object sets that include both diffuse, reflective and transparent materials, although they are very common in domestic scenarios. We show that a combination of cues from multiple sensor modalities, including specular reflectance and unavailable depth information, allows us to capture a larger subset of household objects by extending a state of the art object recognition method. This leads to a significant increase in robustness of recognition over a larger set of commonly used objects.Comment: 12 page

    Fabrication of Isolated Iron Nanowires

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    Nanoscale interconnects are an important component of molecular electronics. Here we use X-ray spectromicroscopy techniques as well as scanning probe methods to explore the self-assembled growth of insulated iron nanowires as a potential means of supplying an earth abundant solution. The intrinsic anisotropy of a TiO2(110) substrate directs the growth of micron length iron wires at elevated temperatures, with a strong metal-support interaction giving rise to ilmenite (FeTiO3) encapsulation. Iron nanoparticles that decorate the nanowires display magnetic properties that suggest other possible applications

    Involvement of Laminin Binding Integrins and Laminin-5 in Branching Morphogenesis of the Ureteric Bud during Kidney Development

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    AbstractBranching morphogenesis of the ureteric bud (UB) [induced by the metanephric mesenchyme (MM)] is necessary for normal kidney development. The role of integrins in this complex developmental process is not well understood. However, the recent advent of in vitro model systems to study branching of UB cells and isolated UB tissue makes possible a more detailed analysis of the integrins involved. We detected integrin subunits α3, α6, β1, and β4 in both the UB and cells derived from the early UB. Blocking the function of each of these integrin subunits individually markedly inhibited branching morphogenesis in cell culture models. However, inhibiting individual integrin function with blocking antibodies in whole kidney and isolated UB culture only partially inhibited UB branching morphogenesis, suggesting that, in these more complex in vitro systems, multiple integrins are involved in the branching program. In whole organ and isolated bud culture, marked retardation of UB branching was observed only when both α3 and α6 integrin subunits were inhibited. The α6 integrin subunit can be expressed as both α6β1 and α6β4, and both of these β subunits are important for UB branching morphogenesis in both cell and organ culture. Furthermore, laminin-5, a common ligand for integrins α3β1 and α6β4, was detected in the developing UB and shown to be required for normal UB branching morphogenesis in whole embryonic kidney organ culture as well as isolated UB culture. Together, these data from UB cell culture, organ culture, and isolated UB culture models indicate that both integrin α3 and α6 subunits play a direct role in UB branching morphogenesis, as opposed to being modulators of the inductive effects of mesenchyme on UB development. Furthermore the data are consistent with a role for laminin-5, acting through its α3β1 and/or α6β4 integrin receptors, in UB branching during nephrogenesis. These data may help to partially explain the renal phenotype seen in integrin α3 and α3/α6 subunit-deficient animals

    Regulation of mammary gland branching morphogenesis by the extracellular matrix and its remodeling enzymes.

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    A considerable body of research indicates that mammary gland branching morphogenesis is dependent, in part, on the extracellular matrix (ECM), ECM-receptors, such as integrins and other ECM receptors, and ECM-degrading enzymes, including matrix metalloproteinases (MMPs) and their inhibitors, tissue inhibitors of metalloproteinases (TIMPs). There is some evidence that these ECM cues affect one or more of the following processes: cell survival, polarity, proliferation, differentiation, adhesion, and migration. Both three-dimensional culture models and genetic manipulations of the mouse mammary gland have been used to study the signaling pathways that affect these processes. However, the precise mechanisms of ECM-directed mammary morphogenesis are not well understood. Mammary morphogenesis involves epithelial 'invasion' of adipose tissue, a process akin to invasion by breast cancer cells, although the former is a highly regulated developmental process. How these morphogenic pathways are integrated in the normal gland and how they become dysregulated and subverted in the progression of breast cancer also remain largely unanswered questions

    The Heterotrimeric Laminin Coiled-Coil Domain Exerts Anti-Adhesive Effects and Induces a Pro-Invasive Phenotype

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    Laminins are large heterotrimeric cross-shaped extracellular matrix glycoproteins with terminal globular domains and a coiled-coil region through which the three chains are assembled and covalently linked. Laminins are key components of basement membranes, and they serve as attachment sites for cell adhesion, migration and proliferation. In this work, we produced a recombinant fragment comprising the entire laminin coiled-coil of the α1-, β1-, and γ1-chains that assemble into a stable heterotrimeric coiled-coil structure independently of the rest of the molecule. This domain was biologically active and not only failed to serve as a substrate for cell attachment, spreading and focal adhesion formation but also inhibited cell adhesion to laminin when added to cells in a soluble form at the time of seeding. Furthermore, gene array expression profiling in cells cultured in the presence of the laminin coiled-coil domain revealed up-regulation of genes involved in cell motility and invasion. These findings were confirmed by real-time quantitative PCR and zymography assays. In conclusion, this study shows for the first time that the laminin coiled-coil domain displays anti-adhesive functions and has potential implications for cell migration during matrix remodeling

    First experimental determination of the radiative-decay probability of the 31− state in ¹²C for estimating the triple alpha reaction rate in high temperature environments

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    The triple alpha reaction is one of the most important reactions in the nuclear astrophysics. However, its reaction rate in high temperature environments at T₉>2 was still uncertain. One of the major origins of the uncertainty was that the radiative-decay probability of the 3⁻₁ state in ¹²C was unknown. In the present work, we have determined the radiative-decay probability of the 3⁻₁ state to be 1.3[+1.2][-1.1] × 10⁻⁶ by measuring the ¹H(¹²C, ¹²Cp) reaction for the first time, and derived the triple alpha reaction rate in high temperature environments from the measured radiative-decay probability. The present result suggests that the 3⁻₁ state noticeably enhances the triple alpha reaction rate although the contribution from the 3⁻₁ state had been assumed to be small

    Establishment and Validation of Computational Model for MT1-MMP Dependent ECM Degradation and Intervention Strategies

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    MT1-MMP is a potent invasion-promoting membrane protease employed by aggressive cancer cells. MT1-MMP localizes preferentially at membrane protrusions called invadopodia where it plays a central role in degradation of the surrounding extracellular matrix (ECM). Previous reports suggested a role for a continuous supply of MT1-MMP in ECM degradation. However, the turnover rate of MT1-MMP and the extent to which the turnover contributes to the ECM degradation at invadopodia have not been clarified. To approach this problem, we first performed FRAP (Fluorescence Recovery after Photobleaching) experiments with fluorescence-tagged MT1-MMP focusing on a single invadopodium and found very rapid recovery in FRAP signals, approximated by double-exponential plots with time constants of 26 s and 259 s. The recovery depended primarily on vesicle transport, but negligibly on lateral diffusion. Next we constructed a computational model employing the observed kinetics of the FRAP experiments. The simulations successfully reproduced our FRAP experiments. Next we inhibited the vesicle transport both experimentally, and in simulation. Addition of drugs inhibiting vesicle transport blocked ECM degradation experimentally, and the simulation showed no appreciable ECM degradation under conditions inhibiting vesicle transport. In addition, the degree of the reduction in ECM degradation depended on the degree of the reduction in the MT1-MMP turnover. Thus, our experiments and simulations have established the role of the rapid turnover of MT1-MMP in ECM degradation at invadopodia. Furthermore, our simulations suggested synergetic contributions of proteolytic activity and the MT1-MMP turnover to ECM degradation because there was a nonlinear and marked reduction in ECM degradation if both factors were reduced simultaneously. Thus our computational model provides a new in silico tool to design and evaluate intervention strategies in cancer cell invasion
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