Hardware-Software Cosynthesis for Run-time Incrementally Reconfigurable FPGAs

This paper presents a method for hardware-software cosynthesis with run-time incrementally reconfigurable FPGAs. To reduce the run-time overhead of reconfiguring FPGAs, we present a concept called early partial reconfiguration (EPR) which minimizes the overhead by performing reconfiguration for an operation (or a task in our terms) mapped to an FPGA as early as possible so that the operation is ready to start when its execution is requested. For further reduction of the overhead, we integrate the incremental reconfiguration (IR) of FPGAs with the EPR concept. We present an ILP formulation and an efficient heuristic algorithm based on the EPR and IR concepts. Experiments on embedded system examples and synthetic examples show the efficiency of the proposed metho

Reduction of Cav1.3 channels in dorsal hippocampus impairs the development of dentate gyrus newborn neurons and hippocampal-dependent memory tasks

Cav1.3 has been suggested to mediate hippocampal neurogenesis of adult mice and contribute to hippocampal-dependent learning and memory processes. However, the mechanism of Cav1.3 contribution in these processes is unclear. Here, roles of Cav1.3 of mouse dorsal hippocampus during newborn cell development were examined. We find that knockout (KO) of Cav1.3 resulted in the reduction of survival of newborn neurons at 28 days old after mitosis. The retroviral eGFP expression showed that both dendritic complexity and the number and length of mossy fiber bouton (MFB) filopodia of newborn neurons at 14 days old were significantly reduced in KO mice. Both contextual fear conditioning (CFC) and object-location recognition tasks were impaired in recent (1 day) memory test while passive avoidance task was impaired only in remote ( 20 days) memory in KO mice. Results using adeno-associated virus (AAV)-mediated Cav1.3 knock-down (KD) or retrovirus-mediated KD in dorsal hippocampal DG area showed that the recent memory of CFC was impaired in both KD mice but the remote memory was impaired only in AAV KD mice, suggesting that Cav1.3 of mature neurons play important roles in both recent and remote CFC memory while Cav1.3 in newborn neurons is selectively involved in the recent CFC memory process. Meanwhile, AAV KD of Cav1.3 in ventral hippocampal area has no effect on the recent CFC memory. In conclusion, the results suggest that Cav1.3 in newborn neurons of dorsal hippocampus is involved in the survival of newborn neurons while mediating developments of dendritic and axonal processes of newborn cells and plays a role in the memory process differentially depending on the stage of maturation and the type of learning task. © 2017 Kim et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

Recent research trends in textile-based temperature sensors: a mini review

In this review, the current state of research on textile-based temperature sensors is explored by focusing on their potential use in various applications. The textile-based sensors show various advantages including flexibility, conformability and seamlessness for the wearer. Integration of the textile-based sensors into clothes or fabric-based products enables continuous and sensitive monitoring of change in temperature, which can be used for various medical and fitness applications. However, there are lacks of comprehensive review on the textile-based temperature sensors. This review introduces various types of textile-based temperature sensors, including resistive, thermoelectric and fibre-optical sensors. In addition, the challenges that need to be addressed to fully realise their potential, which include improving sensitivity and accuracy, integrating wireless communication capabilities, and developing low-cost fabrication techniques. The technological advances in textile-based temperature sensors to overcome the limitations will revolutionize wearable devices requiring function of temperature monitoring

Reduction of Ca_v1.3 channels in dorsal hippocampus impairs the development of dentate gyrus newborn neurons and hippocampal-dependent memory tasks

<div><p>Ca_v1.3 has been suggested to mediate hippocampal neurogenesis of adult mice and contribute to hippocampal-dependent learning and memory processes. However, the mechanism of Ca_v1.3 contribution in these processes is unclear. Here, roles of Ca_v1.3 of mouse dorsal hippocampus during newborn cell development were examined. We find that knock-out (KO) of Ca_v1.3 resulted in the reduction of survival of newborn neurons at 28 days old after mitosis. The retroviral eGFP expression showed that both dendritic complexity and the number and length of mossy fiber bouton (MFB) filopodia of newborn neurons at ≥ 14 days old were significantly reduced in KO mice. Both contextual fear conditioning (CFC) and object-location recognition tasks were impaired in recent (1 day) memory test while passive avoidance task was impaired only in remote (≥ 20 days) memory in KO mice. Results using adeno-associated virus (AAV)-mediated Ca_v1.3 knock-down (KD) or retrovirus-mediated KD in dorsal hippocampal DG area showed that the recent memory of CFC was impaired in both KD mice but the remote memory was impaired only in AAV KD mice, suggesting that Ca_v1.3 of mature neurons play important roles in both recent and remote CFC memory while Ca_v1.3 in newborn neurons is selectively involved in the recent CFC memory process. Meanwhile, AAV KD of Ca_v1.3 in ventral hippocampal area has no effect on the recent CFC memory. In conclusion, the results suggest that Ca_v1.3 in newborn neurons of dorsal hippocampus is involved in the survival of newborn neurons while mediating developments of dendritic and axonal processes of newborn cells and plays a role in the memory process differentially depending on the stage of maturation and the type of learning task.</p></div

Requirement of Split ends for Epigenetic Regulation of Notch Signal-Dependent Genes during Infection-Induced Hemocyte Differentiation▿ †

Drosophila producing a mutant form of the putative transcription coregulator, Split ends (Spen), originally identified in the analysis of neuronal development, display diverse immune defects. In order to understand the role of Spen in the innate immune response, we analyzed the transcriptional defects associated with spen mutant hemocytes and their relationship to the Notch signaling pathways. Spen is regulated by the Notch pathway in the lymph glands and is required for Notch-dependent activation of a large number of genes involved in energy metabolism and differentiation. Analysis of the epigenetic marks associated with Spen-dependent genes indicates that Spen performs its function as a coactivator by regulating chromatin modification. Intriguingly, expression of the Spen-dependent genes was transiently downregulated in a Notch-dependent manner by the Dif activated upon recognition of pathogen-associated molecules, demonstrating the existence of cross talk between hematopoietic regulation and the innate immune response. Our observations reveal a novel connection between the Notch and Toll/IMD signaling pathways and demonstrate a coactivating role for Spen in activating Notch-dependent genes in differentiating cells

Impairments of hippocampus-dependent memory tasks in Ca_v1.3 KO mice.

<p>(A) Scheme of CFC learning and memory tests. Both recent and remote CFC memories were assessed in the same chamber at Days 0, 1, 2 and 23. (B) Freezing responses of CFC memory tasks. (Day 0, WT, 0 ± 0, n = 5, KO, 0 ± 0, n = 5; Day 1, WT, 39.80 ± 3.33%, n = 15, KO, 8.39 ± 1.40%, n = 11, <i>p</i> < 0.00001; Day 2, WT, 59.59 ± 5.60%, n = 13, KO, 47.18 ± 2.74%, n = 9, <i>p</i> = 0.098; Day 23, WT, 56.75 ± 4.58%, n = 10, KO, 38.74 ± 14.30%, n = 6, p = 0.305). *, **, *** indicate <i>p</i> < 0.05, <i>p</i> < 0.01, <i>p</i> < 0.001, respectively, unless otherwise mentioned. Two-way ANOVA, F_G = 18.24, <i>p</i> = 0.000; F_T = 17.88, <i>p</i> = 0.000; F_G+T = 2.31, <i>p</i> = 0.106. (C) Scheme of PA tasks. (D) Latency of entrance to dark room of PA tasks. (Day 0, WT, 13.13 ± 2.88 s, n = 24, KO, 13.12 ± 1.75 s, n = 24, <i>p</i> = 0.990; Day 1, WT, 268.89 ± 16.18 s, n = 24, KO, 239.34 ± 20.72 s, n = 24, <i>p</i> = 0.267; Day 21, WT, 241.38 ± 28.90 s, n = 13, KO, 294.95 ± 5.05 s, n = 13, <i>p</i> = 0.080; Day 42, WT, 232.67 ± 34.10 s, n = 9, KO, 107.22 ± 27.86 s, n = 12, <i>p</i> = 0.010; Day 63, WT, 224.59 ± 34.76 s, n = 7, KO, 46.29 ± 10.71 s, n = 10, <i>p</i> = 0.000). Two-way ANOVA, F_G = 2.45, <i>p</i> = 0.12; F_T = 17.47, <i>p</i> = 0.00; F_G+T = 2.33, <i>p</i> = 0.08. (E) Schemes of OR and OLR tasks. (F) Preference index measurement of OR/OLR tasks. (OR task: WT, 76.41 ± 1.66%, n = 11, KO, 72.54 ± 4.0%, n = 9, <i>p</i> = 0.339; OLR task: WT, 55.19 ± 4.04%, n = 11, KO, 42.89 ± 4.13%, n = 9, <i>p</i> = 0.048).</p

Effects of Ca_v1.3 KO on developments of dendrites, spines and MFB filopodia of DG newborn neurons.

<p>(A) Confocal images of GFP (+) neurons at 14 and 28 days after GFP-retroviral infection. <i>Scale bar</i>, 50 μm. (B-E) Quantification of dendritic development. *, **, *** indicate <i>p</i> < 0.05, <i>p</i> < 0.01, <i>p</i> < 0.001, respectively. (B) Total number of dendritic branching points at 14 and 28 days after viral infection. (Day 14, WT, 7.64 ± 0.41, n = 62, KO, 6.55 ± 0.25, n = 102, <i>p</i> = 0.017; Day 28, WT, 5.71 ± 0.20, n = 107, KO, 4.20 ± 0.18, n = 120, <i>p</i> < 0.00001, n = 3 animals per group). Two-way ANOVA, F_G = 26.96, <i>p</i> = 0.000; F_T = 73.08, <i>p</i> = 0.000; F_G+T = 0.68, <i>p</i> = 0.001. (C) Total dendritic length measurement at 14 and 28 days after viral injection. (Day 14, WT, 328.35 ± 14.57 μm, n = 69, KO, 362.34 ± 45.06 μm, n = 100, <i>p</i> = 0.12; Day 28, WT, 552.90 ± 19.15 μm, n = 107, KO, 466.34 ± 19.97 μm, n = 119, n = 4 animals per group, <i>p</i> = 0.002). Two-way ANOVA, F_G = 1.96, <i>p</i> = 0.162; F_T = 76.56, <i>p</i> = 0.000; F_G+T = 10.31, <i>p</i> = 0.001. (D-E) Number of dendritic crossings in Sholl analysis at 14 (D) and 28 days (E) after viral infection. (Day 28: 10 μm, WT, 1.29 ± 0.07, KO, 1.13 ± 0.04, <i>p</i> = 0.022; 20 μm, WT, 1.70 ± 0.10, KO, 1.39 ± 0.07, <i>p</i> = 0.011; 30 μm, WT, 2.30 ± 0.13, KO, 1.81 ± 0.09, <i>p</i> = 0.001; 40 μm, WT, 3.13 ± 0.16, KO, 2.44 ± 0.11, <i>p</i> = 0.001; 50 μm, WT, 3.69 ± 0.18, KO, 3.03 ± 0.13, <i>p</i> = 0.004; 60 μm, WT, 3.75 ± 0.18, KO, 3.15 ± 0.14, <i>p</i> = 0.010; 70 μm, WT, 3.73 ± 0.19, KO, 3.21 ± 0.15, <i>p</i> = 0.025; 80 μm, WT, 3.65 ± 0.16, KO, 2.98 ± 0.14, <i>p</i> = 0.005; 90 μm, WT, 3.49 ± 0.15, KO, 2.96 ± 0.15, <i>p</i> = 0.013; WT, n = 107 cells, KO, n = 122 cells, n = 4 animals per group). Two-way ANOVA, F_G = 10.54, <i>p</i> = 0.001; F_T = 27.18, <i>p</i> = 0.000; F_D = 92.87, <i>p</i> = 0.000; F_G+T = 34.97, <i>p</i> = 0.000; F_G+D = 1.23, <i>p</i> = 0.27; F_T+D = 23.76, <i>p</i> = 0.000; F_G+T+D = 0.92, <i>p</i> = 0.504. (F) <i>Left</i>, representative image (60x) of newborn neurons at 28 days after GFP-retroviral infection. Red, DAPI. White rectangle shows a distal dendritic region of a newborn neuron of Ca_v1.3 WT mice for spine analysis. <i>Right</i>, exemplary high magnification (60x/6x-zoom) images (<i>top</i>) and 3D reconstruction images (<i>bottom</i>) of a distal dendritic region of a newborn neuron of WT and Ca_v1.3 KO mice. White arrows indicate stubby spines, yellow arrows indicate mushroom spines and red arrows indicate thin spines. <i>Scale bar</i>, 50 μm (60x), 5 μm (60x/6x-zoom) and 2 μm (3D image). (G) Spine density plot for each type of spines. (Thin spines, WT, 0.82 ± 0.07 spines/μm, KO, 0.83 ± 0.06 spines/μm, <i>p</i> = 0.434; stubby spines, WT, 1.10 ± 0.07 spines/μm, KO, 0.95 ± 0.05 spines/μm, <i>p</i> = 0.064; mushroom spines, WT, 0.14 ± 0.017 spines/μm, KO, 0.20 ± 0.06 spines/μm, <i>p</i> = 0.409, WT, n = 28 cells, KO, n = 29 cells, n = 2 animals per group). (H) <i>Top</i>, confocal images of CA3 region axonal fibers of newborn neurons at 28 days after GFP expressing retrovirus injection. Red, DAPI. <i>Bottom</i>, high magnification images of axonal boutons near CA3 pyramidal cell layer. White and yellow arrows indicate boutons and filopodia, respectively. <i>Insets</i>, 3D image of bouton and filopodia. <i>Scale bars</i>, 50 μm (40x), 10 μm (40x/6x-zoom), 5 μm (<i>insets</i>). (I) Size of mossy fiber boutons (WT, 11.52 ± 0.47, n = 84 boutons; KO, 10.07 ± 0.45, n = 70 boutons, n = 3 animals per group, <i>p</i> = 0.029). (J) Total number of filopodia of axonal boutons (WT, 3.98 ± 0.25, n = 53 boutons, KO, 3.2 ± 0.19, n = 65 boutons, n = 3 animals per group, <i>p</i> = 0.010) and (K) the length of filopodia of axonal boutons (WT, 25.99 ± 2.02 μm, n = 53 boutons, KO, 19.16 ± 1.29 μm, n = 65 boutons, n = 3 animals per group, <i>p</i> = 0.004).</p