Weak local rules for planar octagonal tilings

We provide an effective characterization of the planar octagonal tilings which admit weak local rules. As a corollary, we show that they are all based on quadratic irrationalities, as conjectured by Thang Le in the 90s.Comment: 23 pages, 6 figure

Fundamental Limits of Low-Density Spreading NOMA with Fading

Spectral efficiency of low-density spreading non-orthogonal multiple access channels in the presence of fading is derived for linear detection with independent decoding as well as optimum decoding. The large system limit, where both the number of users and number of signal dimensions grow with fixed ratio, called load, is considered. In the case of optimum decoding, it is found that low-density spreading underperforms dense spreading for all loads. Conversely, linear detection is characterized by different behaviors in the underloaded vs. overloaded regimes. In particular, it is shown that spectral efficiency changes smoothly as load increases. However, in the overloaded regime, the spectral efficiency of low- density spreading is higher than that of dense spreading

Exploring Deep Space: Learning Personalized Ranking in a Semantic Space

Recommender systems leverage both content and user interactions to generate recommendations that fit users' preferences. The recent surge of interest in deep learning presents new opportunities for exploiting these two sources of information. To recommend items we propose to first learn a user-independent high-dimensional semantic space in which items are positioned according to their substitutability, and then learn a user-specific transformation function to transform this space into a ranking according to the user's past preferences. An advantage of the proposed architecture is that it can be used to effectively recommend items using either content that describes the items or user-item ratings. We show that this approach significantly outperforms state-of-the-art recommender systems on the MovieLens 1M dataset.Comment: 6 pages, RecSys 2016 RSDL worksho

Words are Malleable: Computing Semantic Shifts in Political and Media Discourse

Recently, researchers started to pay attention to the detection of temporal shifts in the meaning of words. However, most (if not all) of these approaches restricted their efforts to uncovering change over time, thus neglecting other valuable dimensions such as social or political variability. We propose an approach for detecting semantic shifts between different viewpoints--broadly defined as a set of texts that share a specific metadata feature, which can be a time-period, but also a social entity such as a political party. For each viewpoint, we learn a semantic space in which each word is represented as a low dimensional neural embedded vector. The challenge is to compare the meaning of a word in one space to its meaning in another space and measure the size of the semantic shifts. We compare the effectiveness of a measure based on optimal transformations between the two spaces with a measure based on the similarity of the neighbors of the word in the respective spaces. Our experiments demonstrate that the combination of these two performs best. We show that the semantic shifts not only occur over time, but also along different viewpoints in a short period of time. For evaluation, we demonstrate how this approach captures meaningful semantic shifts and can help improve other tasks such as the contrastive viewpoint summarization and ideology detection (measured as classification accuracy) in political texts. We also show that the two laws of semantic change which were empirically shown to hold for temporal shifts also hold for shifts across viewpoints. These laws state that frequent words are less likely to shift meaning while words with many senses are more likely to do so.Comment: In Proceedings of the 26th ACM International on Conference on Information and Knowledge Management (CIKM2017

Hamiltonian lattice QCD at finite chemical potential

At sufficiently high temperature and density, quantum chromodynamics (QCD) is expected to undergo a phase transition from the confined phase to the quark-gluon plasma phase. In the Lagrangian lattice formulation the Monte Carlo method works well for QCD at finite temperature, however, it breaks down at finite chemical potential. We develop a Hamiltonian approach to lattice QCD at finite chemical potential and solve it in the case of free quarks and in the strong coupling limit. At zero temperature, we calculate the vacuum energy, chiral condensate, quark number density and its susceptibility, as well as mass of the pseudoscalar, vector mesons and nucleon. We find that the chiral phase transition is of first order, and the critical chemical potential is $\mu_C =m_{dyn}^{(0)}$ (dynamical quark mass at $\mu=0$). This is consistent with $\mu_C \approx M_N^{(0)}/3$ (where $M_N^{(0)}$ is the nucleon mass at $\mu=0$).Comment: Final version appeared in Phys. Rev.

DPSCs from Inflamed Pulp Modulate Macrophage Function via the TNF-α/IDO Axis

Human dental pulp stem cells (DPSCs) can be isolated from inflamed pulp derived from carious teeth with symptomatic irreversible pulpitis (I-DPSCs), which possess stemness and multidifferentiation potentials similar to DPSCs from healthy pulp. Since macrophages—essential cell players of the pulpal innate immunity—can regulate pulpal inflammation and repair, the authors investigated the immunomodulatory effects of DPSCs/I-DPSCs on macrophage functions and their underlying mechanisms. Similar to DPSCs, I-DPSCs were capable of colony-forming efficiency and adipogenic and osteo/dentinogenic differentiation under in vitro induction conditions. I-DPSCs also expressed a similar phenotypic profile of mesenchymal stem cell markers, except a relatively higher level of CD146 as compared with DPSCs. Coculture of DPSCs or I-DPSCs with differentiated THP-1 cells, the human monocyte cell line, markedly suppressed tumor necrosis factor α (TNF-α) secretion in response to stimulation with lipopolysaccharides (LPS) and/or nigericin. However, unlike TNF-α, the secreted level of interleukin 1β was not affected by coculture with DPSCs or I-DPSCs. Furthermore, DPSC/I-DPSC-mediated inhibition of TNF-α secretion by macrophages was abolished by pretreatment with 1-methyl-D-tryptophan, a specific inhibitor of indoleamine-pyrrole 2,3-dioxygenase (IDO), but not by NSC-398, a specific inhibitor of COX-2, suggesting IDO as a mediator. Interestingly, IDO expression was significantly augmented in macrophages and mesenchymal stromal cells in inflamed human pulp tissues. Collectively, these findings show that I-DPSCs, similar to DPSCs, possess stem cell properties and suppress macrophage functions via the TNF-α/IDO axis, thereby providing a physiologically relevant context for their innate immunomodulatory activity in the dental pulp and their capability for pulp repair

Direct genetic demonstration of Gα13 coupling to the orphan G protein-coupled receptor G2A leading to RhoA-dependent actin rearrangement

G2A is an orphan G protein-coupled receptor (GPCR), expressed predominantly in T and B cells and homologous to a small group of GPCRs of unknown function expressed in lymphoid tissues. G2A is transcriptionally induced in response to diverse stimuli, and its ectopic expression suppresses transformation of B lymphoid precursors by BCR-ABL. G2A induces morphological transformation of NIH 3T3 fibroblasts. Microinjection of constructs encoding G2A into Swiss 3T3 fibroblasts induces actin reorganization into stress fibers that depends on RhoA, but not CDC42 or RAC. G2A elicits RhoA-dependent transcriptional activation of serum response factor. Direct evaluation of RhoA activity demonstrates elevated levels of RhoA-GTP in G2A-expressing cells. Microinjection of embryonic fibroblasts derived from various Galpha knockout mice establishes a requirement for Galpha 13 but not Galpha 12 or Galpha q/11 in G2A-induced actin rearrangement. In conclusion, G2A represents a family of GPCRs expressed in lymphocytes that may link diverse stimuli to cytoskeletal reorganization and transcriptional activation through a pathway involving Galpha 13 and RhoA