129 research outputs found

    A branch connection rule of one-way rail network

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    We deal with network inspired by toy train, which is constructed by connecting Y-shaped branches. A train passes a branch through either of splitted rails and not allowed to go backward. Under these assumptions, we consider unidirectionality of a rail network, that is, there is a orientation of the rail network such that any trail of a train starting with the direction does not contradict to the orientation. We find that a rail network is one-way if and only if a digraph derived from the rail network is disconnected, which is also equal to no existence of cycle which contains odd number of tracks connecting the same side of branches

    Automated analysis of Physarum network structure and dynamics

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    We evaluate different ridge-enhancement and segmentation methods to automatically extract the network architecture from time-series of Physarum plasmodia withdrawing from an arena via a single exit. Whilst all methods gave reasonable results, judged by precision-recall analysis against a ground-truth skeleton, the mean phase angle (Feature Type) from intensity-independent, phase-congruency edge enhancement and watershed segmentation was the most robust to variation in threshold parameters. The resultant single pixel-wide segmented skeleton was converted to a graph representation as a set of weighted adjacency matrices containing the physical dimensions of each vein, and the inter-vein regions. We encapsulate the complete image processing and network analysis pipeline in a downloadable software package, and provide an extensive set of metrics that characterise the network structure, including hierarchical loop decomposition to analyse the nested structure of the developing network. In addition, the change in volume for each vein and intervening plasmodial sheet was used to predict the net flow across the network. The scaling relationships between predicted current, speed and shear force with vein radius were consistent with predictions from Murray's law. This work was presented at PhysNet 2015

    Enhancing the antitumor activity of ErbB blockade with histone deacetylase (HDAC) inhibition

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    Molecular inhibition of the ErbB signaling pathway represents a promising cancer treatment strategy. Preclinical studies suggest that enhancement of antitumor activity can be achieved by maximizing ErbB signaling inhibition. Using cDNA microarrays, we identified histone deacetylase (HDAC) inhibitors as having strong potential to enhance the effects of anti‐ErbB agents. Studies using a 20,000 element (20K) cDNA microarray demonstrate decreased transcript expression of ErbB1 (epidermal growth factor receptor) and ErbB2 in DU145 (prostate) and ErbB2 in SKBr3 (breast) cancer cell lines. Additional changes in the DU145 gene expression profile with potential interaction to ErbB signaling include down‐regulation of caveolin‐1 and hypoxia inducible factor 1‐α (HIF1‐α), and up‐regulation of gelsolin, p19(INK4D) and Nur77. Findings were validated using real time RT‐PCR and Western blot analysis. Enhanced proliferative inhibition, apoptosis induction and signaling inhibition were demonstrated when combining HDAC inhibition with ErbB blockade. These results suggest that used cooperatively, anti‐ErbB agents and HDAC inhibitors may offer a promising strategy of dual targeted therapy. Additionally, microarray data suggest that the beneficial interaction of these agents may not derive solely from modulation of ErbB expression, but may result from effects on other oncogenic processes including angiogenesis, invasion and cell cycle kinetics. © 2005 Wiley‐Liss, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/94461/1/21465_ftp.pd

    Control of Length and Spatial Functionality of Single-Wall Carbon Nanotube AFM Nanoprobes

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    Single-wall carbon nanotube (SWNT) nanofibrils were assembled onto conductive atomic force microscopy (AFM) probes with the help of dielectrophoresis (DEP). This process involved the application of a 10 V, 2 MHz, AC bias between a metal-coated AFM probe and a dilute suspension of SWNTs. This exerted a positive dielectrophoretic force onto the nanotubes that caused them to align while precipitating out onto the probe. The gradual removal of the AFM probe away from the SWNT suspension consolidated these nanotubes into nanofibrils with a high degree of alignment as demonstrated with polarization Raman experiments. By varying the pulling speed, immersion time, and concentration of the SWNT suspension, one can tailor the diameter and thus the stiffness of these probes. Precise length trimming of these nanofibrils was also performed by their gradual immersion and dissolution into a liquid that strongly interacted with nanotubes, (i.e., sodium dodecyl sulfate (SDS) solution). Vacuum annealing these nanoprobes at temperature up to 450 degree C further increased their stiffness and rendered them insoluble to SDS and all other aqueous media. Regrowth of a new SWNT nanofibril from the side or at the end of a previously grown SWNT nanofibril was also demonstrated by a repeated dielectrophoretic assembly at the desired immersion depth. These SWNT nanofibril-equipped AFM probes are electrically conductive and mechanically robust for use as high-aspect-ratio electrochemical nanoprobes

    The “Goldilocks Zoneâ€? from a redox perspectiveâ€â€�Adaptive vs. deleterious responses to oxidative stress in striated muscle

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    Consequences of oxidative stress may be beneficial or detrimental in physiological systems. An organ system's position on the “hormetic curve� is governed by the source and temporality of reactive oxygen species (ROS) production, proximity of ROS to moieties most susceptible to damage, and the capacity of the endogenous cellular ROS scavenging mechanisms. Most importantly, the resilience of the tissue (the capacity to recover from damage) is a decisive factor, and this is reflected in the disparate response to ROS in cardiac and skeletal muscle. In myocytes, a high oxidative capacity invariably results in a significant ROS burden which in homeostasis, is rapidly neutralized by the robust antioxidant network. The up-regulation of key pathways in the antioxidant network is a central component of the hormetic response to ROS. Despite such adaptations, persistent oxidative stress over an extended time-frame (e.g., months to years) inevitably leads to cumulative damages, maladaptation and ultimately the pathogenesis of chronic diseases. Indeed, persistent oxidative stress in heart and skeletal muscle has been repeatedly demonstrated to have causal roles in the etiology of heart disease and insulin resistance, respectively. Deciphering the mechanisms that underlie the divergence between adaptive and maladaptive responses to oxidative stress remains an active area of research for basic scientists and clinicians alike, as this would undoubtedly lead to novel therapeutic approaches. Here, we provide an overview of major types of ROS in striated muscle and the divergent adaptations that occur in response to them. Emphasis is placed on highlighting newly uncovered areas of research on this topic, with particular focus on the mitochondria, and the diverging roles that ROS play in muscle health (e.g., exercise or preconditioning) and disease (e.g., cardiomyopathy, ischemia, metabolic syndrome)

    Stem Cell Therapy: Pieces of the Puzzle

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    Acute ischemic injury and chronic cardiomyopathies can cause irreversible loss of cardiac tissue leading to heart failure. Cellular therapy offers a new paradigm for treatment of heart disease. Stem cell therapies in animal models show that transplantation of various cell preparations improves ventricular function after injury. The first clinical trials in patients produced some encouraging results, despite limited evidence for the long-term survival of transplanted cells. Ongoing research at the bench and the bedside aims to compare sources of donor cells, test methods of cell delivery, improve myocardial homing, bolster cell survival, and promote cardiomyocyte differentiation. This article reviews progress toward these goals

    Tumor cell survival pathways activated by photodynamic therapy: a molecular basis for pharmacological inhibition strategies

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