Maximizing Friend-Making Likelihood for Social Activity Organization

The social presence theory in social psychology suggests that computer-mediated online interactions are inferior to face-to-face, in-person interactions. In this paper, we consider the scenarios of organizing in person friend-making social activities via online social networks (OSNs) and formulate a new research problem, namely, Hop-bounded Maximum Group Friending (HMGF), by modeling both existing friendships and the likelihood of new friend making. To find a set of attendees for socialization activities, HMGF is unique and challenging due to the interplay of the group size, the constraint on existing friendships and the objective function on the likelihood of friend making. We prove that HMGF is NP-Hard, and no approximation algorithm exists unless P = NP. We then propose an error-bounded approximation algorithm to efficiently obtain the solutions very close to the optimal solutions. We conduct a user study to validate our problem formulation and per- form extensive experiments on real datasets to demonstrate the efficiency and effectiveness of our proposed algorithm

GCN-RL Circuit Designer: Transferable Transistor Sizing with Graph Neural Networks and Reinforcement Learning

Automatic transistor sizing is a challenging problem in circuit design due to the large design space, complex performance trade-offs, and fast technological advancements. Although there has been plenty of work on transistor sizing targeting on one circuit, limited research has been done on transferring the knowledge from one circuit to another to reduce the re-design overhead. In this paper, we present GCN-RL Circuit Designer, leveraging reinforcement learning (RL) to transfer the knowledge between different technology nodes and topologies. Moreover, inspired by the simple fact that circuit is a graph, we learn on the circuit topology representation with graph convolutional neural networks (GCN). The GCN-RL agent extracts features of the topology graph whose vertices are transistors, edges are wires. Our learning-based optimization consistently achieves the highest Figures of Merit (FoM) on four different circuits compared with conventional black-box optimization methods (Bayesian Optimization, Evolutionary Algorithms), random search, and human expert designs. Experiments on transfer learning between five technology nodes and two circuit topologies demonstrate that RL with transfer learning can achieve much higher FoMs than methods without knowledge transfer. Our transferable optimization method makes transistor sizing and design porting more effective and efficient.Comment: Accepted to the 57th Design Automation Conference (DAC 2020); 6 pages, 8 figure

Mutations in PNKD causing paroxysmal dyskinesia alters protein cleavage and stability.

Paroxysmal non-kinesigenic dyskinesia (PNKD) is a rare autosomal dominant movement disorder triggered by stress, fatigue or consumption of either alcohol or caffeine. Attacks last 1-4 h and consist of dramatic dystonia and choreoathetosis in the limbs, trunk and face. The disease is associated with single amino acid changes (A7V or A9V) in PNKD, a protein of unknown function. Here we studied the stability, cellular localization and enzymatic activity of the PNKD protein in cultured cells and transgenic animals. The N-terminus of the wild-type (WT) long PNKD isoform (PNKD-L) undergoes a cleavage event in vitro, resistance to which is conferred by disease-associated mutations. Mutant PNKD-L protein is degraded faster than the WT protein. These results suggest that the disease mutations underlying PNKD may disrupt protein processing in vivo, a hypothesis supported by our observation of decreased cortical Pnkd-L levels in mutant transgenic mice. Pnkd is homologous to a superfamily of enzymes with conserved β-lactamase domains. It shares highest homology with glyoxalase II but does not catalyze the same reaction. Lower glutathione levels were found in cortex lysates from Pnkd knockout mice versus WT littermates. Taken together, our results suggest an important role for the Pnkd protein in maintaining cellular redox status

A robust clustering procedure for fuzzy data

AbstractIn this paper we propose a robust clustering method for handling LR-type fuzzy numbers. The proposed method based on similarity measures is not necessary to specify the cluster number and initials. Several numerical examples demonstrate the effectiveness of the proposed robust clustering method, especially robust to outliers, different cluster shapes and initial guess. We then apply this algorithm to three real data sets. These are Taiwanese tea, student data and patient blood pressure data sets. Because tea evaluation comes under an expert subjective judgment for Taiwanese tea, the quality levels are ambiguity and imprecision inherent to human perception. Thus, LR-type fuzzy numbers are used to describe these quality levels. The proposed robust clustering method successfully establishes a performance evaluation system to help consumers better understand and choose Taiwanese tea. Similarly, LR-type fuzzy numbers are also used to describe data types for student and patient blood pressure data. The proposed method actually presents good clustering results for these real data sets

Stemness factor Sall4 is required for DNA damage response in embryonic stem cells.

Mouse embryonic stem cells (ESCs) are genetically more stable than somatic cells, thereby preventing the passage of genomic abnormalities to their derivatives including germ cells. The underlying mechanisms, however, remain largely unclear. In this paper, we show that the stemness factor Sall4 is required for activating the critical Ataxia Telangiectasia Mutated (ATM)-dependent cellular responses to DNA double-stranded breaks (DSBs) in mouse ESCs and confer their resistance to DSB-induced cytotoxicity. Sall4 is rapidly mobilized to the sites of DSBs after DNA damage. Furthermore, Sall4 interacts with Rad50 and stabilizes the Mre11-Rad50-Nbs1 complex for the efficient recruitment and activation of ATM. Sall4 also interacts with Baf60a, a member of the SWI/SNF (switch/sucrose nonfermentable) ATP-dependent chromatin-remodeling complex, which is responsible for recruiting Sall4 to the site of DNA DSB damage. Our findings provide novel mechanisms to coordinate stemness of ESCs with DNA damage response, ensuring genomic stability during the expansion of ESCs

1999-2000 Master Class - Kemal Gekic (Piano)

https://spiral.lynn.edu/conservatory_masterclasses/1190/thumbnail.jp