Double Object Constructions in Korean: Asymmetry between Theme and Goal

Much of the generative studies on the double object constructions in English have shown that there exists an asymmetrical c-command relation between the Theme argument and the Goal argument: the Goal uniformly c-commands the Theme at D-structure. This paper attempts to prove that Korean also exhibits an asymmetric relation between the Theme and Goal in double object constructions, but it is the Theme that asymmetrically c-commands the Goal at D-structure in Korean

Analog Weights in ReRAM DNN Accelerators

Artificial neural networks have become ubiquitous in modern life, which has triggered the emergence of a new class of application specific integrated circuits for their acceleration. ReRAM-based accelerators have gained significant traction due to their ability to leverage in-memory computations. In a crossbar structure, they can perform multiply-and-accumulate operations more efficiently than standard CMOS logic. By virtue of being resistive switches, ReRAM switches can only reliably store one of two states. This is a severe limitation on the range of values in a computational kernel. This paper presents a novel scheme in alleviating the single-bit-per-device restriction by exploiting frequency dependence of v-i plane hysteresis, and assigning kernel information not only to the device conductance but also partially distributing it to the frequency of a time-varying input. We show this approach reduces average power consumption for a single crossbar convolution by up to a factor of x16 for an unsigned 8-bit input image, where each convolutional process consumes a worst-case of 1.1mW, and reduces area by a factor of x8, without reducing accuracy to the level of binarized neural networks. This presents a massive saving in computing cost when there are many simultaneous in-situ multiply-and-accumulate processes occurring across different crossbars.Comment: 2019 IEEE International Conference on Artificial Intelligence Circuits and Systems, 5 pages, 4 figure

Growth differentiation factor 11 locally controls anterior-posterior patterning of the axial skeleton.

Growth and differentiation factor 11 (GDF11) is a transforming growth factor β family member that has been identified as the central player of anterior-posterior (A-P) axial skeletal patterning. Mice homozygous for Gdf11 deletion exhibit severe anterior homeotic transformations of the vertebrae and craniofacial defects. During early embryogenesis, Gdf11 is expressed predominantly in the primitive streak and tail bud regions, where new mesodermal cells arise. On the basis of this expression pattern of Gdf11 and the phenotype of Gdf11 mutant mice, it has been suggested that GDF11 acts to specify positional identity along the A-P axis either by local changes in levels of signaling as development proceeds or by acting as a morphogen. To further investigate the mechanism of action of GDF11 in the vertebral specification, we used a Cdx2-Cre transgene to generate mosaic mice in which Gdf11 expression is removed in posterior regions including the tail bud, but not in anterior regions. The skeletal analysis revealed that these mosaic mice display patterning defects limited to posterior regions where Gdf11 expression is deficient, whereas displaying normal skeletal phenotype in anterior regions where Gdf11 is normally expressed. Specifically, the mosaic mice exhibited seven true ribs, a pattern observed in wild-type (wt) mice (vs. 10 true ribs in Gdf11-/- mice), in the anterior axis and nine lumbar vertebrae, a pattern observed in Gdf11 null mice (vs. six lumbar vertebrae in wt mice), in the posterior axis. Our findings suggest that GDF11, rather than globally acting as a morphogen secreted from the tail bud, locally regulates axial vertebral patterning

High Extracellular Calcium Increased Expression of Ank, PC-1 andOsteopontin in Mouse Calvarial Cells

In the process of bone remodeling, mineral phase of bone is dissolved by osteoclasts, resulting in elevation of calcium concentration in micro-environment. This study was performed to explore the effect of high extracellular calcium (Ca 2+ e) on mineralized nodule formation and on the expression of progressive ankylosis (Ank), plasma cell membrane glycoprotein-1 (PC-1) and osteopontin by primary cultured mouse calvarial cells. Osteoblastic differentiation and mineralized nodule formation was induced by culture of mouse calvarial cells in osteoblast differentiation medium containing ascorbic acid and β-glycerophosphate. Although Ank, PC-1 and osteopontin are well known inhibitors of mineralization, expression of these genes were induced at the later stage of osteoblast differentiation during when expression of osteocalcin, a late marker gene of osteoblast differentiation, was induced and mineralization was actively progressing. High Ca 2+ e (10 mM) treatment highly enhanced mRNA expression of Ank, PC-1 and osteopontin in the late stage of osteoblast differentiation but not in the early stage. Inhibition of p44/42 MAPK activation but not that of protein kinase C suppressed high Ca 2+ e-induced expression of Ank, PC-1 and osteopontin. When high Ca 2+ e (5 mM or 10 mM) was present in culture medium during when mineral deposition was actively progressing, matrix calcifiation was significantly increased by high Ca 2+ e. This stimulatory effect was abolished by pyrophosphate (5 mM) or levamisole (0.1-0.5 mM), an alkaline phosphatase inhibitor. In addition, probenecid (2mM), an inhibitor of Ank, suppressed matrix calcification in both control and high Ca 2+ e-treated group, suggesting the possible role of Ank in matrix calcification by osteoblasts. Taken together, these results showed that high Ca 2+ e stimulates expression of Ank, PC-1 and osteopontin as well as matrix calcification in late differentiation stage of osteoblasts and that p44/42 MAPK activation is involved in high Ca 2+ e- induced expression of Ank, PC-1 and osteopontin

Comparative Evaluation of Nanofibrous Scaffolding for Bone Regeneration in Critical-Size Calvarial Defects

In a previous study we found that nanofibrous poly(l-lactic acid) (PLLA) scaffolds mimicking collagen fibers in size were superior to solid-walled scaffolds in promoting osteoblast differentiation and bone formation in vitro. In this study we used an in vivo model to confirm the biological properties of nanofibrous PLLA scaffolds and to evaluate how effectively they support bone regeneration against solid-walled scaffolds. The scaffolds were implanted in critical-size defects made on rat calvarial bones. Compared with solid-walled scaffolds, nanofibrous scaffolds supported substantially more new bone tissue formation, which was confirmed by micro-computed tomography measurement and von Kossa staining. Goldner's trichrome staining showed abundant collagen deposition in nanofibrous scaffolds but not in the control solid-walled scaffolds. The cells in these scaffolds were immuno-stained strongly for Runx2 and bone sialoprotein (BSP). In contrast, solid-walled scaffolds implanted in the defects were stained weakly with trichrome, Runx2, and BSP. These in vivo results demonstrate that nanofibrous architecture enhances osteoblast differentiation and bone formation.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/78127/1/ten.tea.2008.0433.pd

The Expression of Matrix Metalloprotease 20 is Stimulated by Wild Type but not by 4 bp- or 2 bp- Deletion Mutant DLX3

Mutations in DLX3 are associated with both autosomal dominant hypoplastic hypomaturation amelogenesis imperfecta (ADHHAI) and tricho-dento-osseous (TDO) syndrome. ADHHAI is caused by a c.561_562delCT (2bpdel DLX3) mutation whereas TDO syndrome is associated with a c.571_574delGGGG (4bp-del DLX3) mutation. However, although the causal relationships between DLX3 and an enamel phenotype have been established, the pathophysiological role of DLX3 mutations in enamel development has not yet been clarified. In our current study, we prepared expression vectors for wild type and deletion mutant DLX3 products (4bp-del DLX3, 2bp-del DLX3) and examined the effects of their overexpression on the expression of the enamel matrix proteins and proteases. Wild type DLX3 enhanced the expression of matrix metalloprotease 20 (MMP20) mRNA and protein in murine ameloblast-like cells. However, neither a 4bp-del nor 2bpdel DLX3 increased MMP20 expression. Wild type DLX3, but not the above DLX3 mutants, also increased the activity of reporters containing 1.5 kb or 0.5 kb of the MMP20 promoter. An examination of protein stability showed that the half-life of wild type DLX3 protein was less than 12 h whilst that of both deletion mutants was longer than 24 h. Endogenous Dlx3 was also found to be continuously expressed during ameloblast differentiation. Since inactivating mutations in the gene encoding MMP20 are associated with amelogenesis imperfecta, the inability of 4bp-del or 2bp-del DLX3 to induce MMP20 expression suggests a possible involvement of such mutations in the enamel phenotype associated with TDO syndrome or ADHHAI

Tricho-dento-osseous Syndrome Mutant Dlx3 Shows Lower Transactivation Potential but Has Longer Half-life than Wild-type Dlx3

Dlx3 is a homeodomain protein and is known to play a role in development and differentiation of many tissues. Deletion of four base pairs in DLX3 (NT3198) is causally related to tricho-dento-osseous (TDO) syndrome (OMIM #190320), a genetic disorder manifested by taurodontism, hair abnormalities, and increased bone density in the cranium. The molecular mechanisms that explain the phenotypic characteristics of TDO syndrome have not been clearly determined. In this study, we examined phenotypic characteristics of wild type DLX3 (wtDlx3) and 4-BP DEL DLX3 (TDO mtDlx3) in C2C12 cells. To investigate how wtDlx3 and TDO mtDlx3 differentially regulate osteoblastic differentiation, reporter assays were performed by using luciferase reporters containing the promoters of alkaline phosphatase, bone sialoprotein or osteocalcin. Both wtDlx3 and TDO mtDlx3 enhanced significantly all the reporter activities but the effect of mtDlx3 was much weaker than that of wtDlx3. In spite of these differences in reporter activity, electrophoretic mobility shift assay showed that both wtDlx3 and TDO mtDlx3 formed similar amounts of DNA binding complexes with Dlx3 binding consensus sequence or with ALP promoter oligonucleotide bearing the Dlx3 binding core sequence. TDO mtDlx3 exhibits a longer half-life than wtDlx3 and it corresponds to PESTfind analysis result showing that potential PEST sequence was missed in carboxy terminal of TDO mtDlx3. In addition, co-immunoprecipitation demonstrated that TDO mtDlx3 binds to Msx2 more strongly than wtDlx3. Taken together, though TDO mtDlx3 acted as a weaker transcriptional activator than wtDlx3 in osteoblastic cells, there is possibility that during in vivo osteoblast differentiation TDO mtDlx3 may antagonize transcriptional repressor activity of Msx2 more effectively and for longer period than wtDlx3, resulting in enhancement of osteoblast differentiation

Fast Large Volume Simulations of the 21 cm Signal from the Reionization and pre-Reionization Epochs

While limited to low spatial resolution, the next generation low-frequency radio interferometers that target 21 cm observations during the era of reionization and prior will have instantaneous fields-of-view that are many tens of square degrees on the sky. Predictions related to various statistical measurements of the 21 cm brightness temperature must then be pursued with numerical simulations of reionization with correspondingly large volume box sizes, of order 1000 Mpc on one side. We pursue a semi-numerical scheme to simulate the 21 cm signal during and prior to Reionization by extending a hybrid approach where simulations are performed by first laying down the linear dark matter density field, accounting for the non-linear evolution of the density field based on second-order linear perturbation theory as specified by the Zel'dovich approximation, and then specifying the location and mass of collapsed dark matter halos using the excursion-set formalism. The location of ionizing sources and the time evolving distribution of ionization field is also specified using an excursion-set algorithm. We account for the brightness temperature evolution through the coupling between spin and gas temperature due to collisions, radiative coupling in the presence of Lyman-alpha photons and heating of the intergalactic medium, such as due to a background of X-ray photons. The hybrid simulation method we present is capable of producing the required large volume simulations with adequate resolution in a reasonable time so a large number of realizations can be obtained with variations in assumptions related to astrophysics and background cosmology that govern the 21 cm signal.Comment: 14 pages and 15 figures. New version to match accepted version for MNRAS. Code available in: http://www.SimFast21.or

Probing the first galaxies with the SKA

Observations of anisotropies in the brightness temperature of the 21 cm line of neutral hydrogen from the period before reionization would shed light on the dawn of the first stars and galaxies. In this paper, we use large-scale semi-numerical simulations to analyse the imprint on the 21 cm signal of spatial fluctuations in the Lyman-alpha flux arising from the clustering of the first galaxies. We show that an experiment such as the Square Kilometer Array (SKA) can probe this signal at the onset of reionization, giving us important information about the UV emission spectra of the first stars and characterizing their host galaxies. SKA-pathfinders with ~ 10% of the full collecting area should be capable of making a statistical detection of the 21 cm power spectrum at redshifts z 67 MHz). We then show that the SKA should be able to measure the three dimensional power spectrum as a function of the angle with the line of sight and discuss the use of the redshift space distortions as a way to separate out the different components of the 21 cm power spectrum. We demonstrate that, at least on large scales where the Lyman-alpha fluctuations are linear, they can be used as a model independent way to extract the power spectra due to these Lyman-alpha fluctuations.Comment: 13 pages, 17 figures. New version to match version accepted by A&A. Improved discussions on the Lyman-alpha simulation, adiabatic cooling fluctuations, the Fisher matrix approach and the Poisson term calculation. New version of the code available at: http://www.SimFast21.or