Pruning based Distance Sketches with Provable Guarantees on Random Graphs

Measuring the distances between vertices on graphs is one of the most fundamental components in network analysis. Since finding shortest paths requires traversing the graph, it is challenging to obtain distance information on large graphs very quickly. In this work, we present a preprocessing algorithm that is able to create landmark based distance sketches efficiently, with strong theoretical guarantees. When evaluated on a diverse set of social and information networks, our algorithm significantly improves over existing approaches by reducing the number of landmarks stored, preprocessing time, or stretch of the estimated distances. On Erd\"{o}s-R\'{e}nyi graphs and random power law graphs with degree distribution exponent $2 < \beta < 3$, our algorithm outputs an exact distance data structure with space between $\Theta(n^{5/4})$ and $\Theta(n^{3/2})$ depending on the value of $\beta$, where $n$ is the number of vertices. We complement the algorithm with tight lower bounds for Erdos-Renyi graphs and the case when $\beta$ is close to two.Comment: Full version for the conference paper to appear in The Web Conference'1

An Empirical Assessment of Characteristics and Optimal Portfolios

We analyze characteristics' joint predictive information through the lens of out-of-sample power utility functions. Linking weights to characteristics to form optimal portfolios suffers from estimation error which we mitigate by maximizing an in-sample loss function that is more concave than the utility function. While no single characteristic can be used to enhance utility by all investors, conditioning on momentum, size, and residual volatility produces portfolios with significantly higher certainty equivalents than benchmarks for all investors. Characteristic complementarities produce the benefits, for example momentum mitigates overfitting inherent in other characteristics. Optimal portfolios' returns lie largely outside the span of traditional factors

Parallel numerical simulation of impact crater with perfect matched layers

Impact craters are the primary geomorphic features on the surfaces of celestial bodies such as the Moon, and their formation has significant implications for the evolutionary history of the celestial body. The study of the impact crater formation process relies mainly on numerical simulation methods, with two-dimensional simulations capable of reproducing general patterns of impact processes while conserving computational resources. However, to mitigate the artificial reflections of shock waves at numerical boundaries, a common approach involves expanding the computational domain, greatly reducing the efficiency of numerical simulations. In this study, we developed a novel two-dimensional code SALEc-2D that employs the perfect matched layer (PML) method to suppress artificial reflections at numerical boundaries. This method enhances computational efficiency while ensuring reliable results. Additionally, we implemented MPI parallel algorithms in the new code to further improve computational efficiency. Simulations that would take over ten hours using the conventional iSALE-2D code can now be completed in less than half an hour using our code, SALEc-2D, on a standard computer. We anticipate that our code will find widespread application in numerical simulations of impact craters in the future.Comment: 17 pages, 8 figure

Seasonality in the cross section of stock returns: Advanced markets versus emerging markets

We extend the studies of stock return seasonality by Heston and Sadka (2008, 2010) to a comprehensive sample of 42 international markets, including 21 advanced markets and 21 emerging markets. The empirical results show a large variation in stock seasonality across markets and suggest that this phenomenon exists primarily in advanced markets. A winner-loser portfolio approach shows that return seasonality is economically significant in advanced markets but not in emerging markets. We conduct statistical, rational and behavioral analyses to explore the potential reasons for the seasonality observed in advanced markets and find that regression bias, the January effect, and the Fama-French-Carhart type risk premium all can partially explain this seasonality difference

Hedge Fund Manager Skill and Style-Shifting

Utilizing a novel style identification procedure, we show that style shifting is a dynamic strategy commonly employed by hedge fund managers. Three quarters of hedge funds shifted their investment styles at least once over the period from January 1994 to December 2013. We perform empirical tests of two hypotheses for the motivations of hedge fund style-shifting, namely backward-looking and forward-looking hypotheses. We find no evidence that style-shifting funds are backward-looking. Instead, we show evidence that managers of style-shifting funds exhibit both style-timing ability and the skill of generating abnormal returns in new styles. The new styles that hedge funds shift to on average outperform their old styles by 0.76% and style-shifting funds on average outperform their new style benchmark by 1.10% over the subsequent 12-month horizon. Finally, we show that small funds, winner funds, and funds with net inflows are more likely to shift styles

NF-kappa B mediated Up-regulation of CCCTC-binding factor in pediatric acute lymphoblastic leukemia

BACKGROUND: Acute lymphoblastic leukemia (ALL) is the most frequently occurring malignant neoplasm in children. Despite advances in treatment and outcomes for ALL patients, the pathogenesis of the disease remains unclear. Microarray analysis of samples from 100 Chinese children with ALL revealed the up-regulation of CTCF (CCCTC binding factor). CTCF is a highly conserved 11-zinc finger protein that is involved in many human cancers; however, the biological function of CTCF in pediatric ALL is unknown. METHODS: The expression patterns of CTCF were evaluated in matched newly diagnosed (ND), complete remission (CR), and relapsed (RE) bone marrow samples from 28 patients. The potential oncogenic mechanism of CTCF and related pathways in leukemogenesis were investigated in leukemia cell lines. RESULTS: We identified significant up-regulation of CTCF in the ND samples. Importantly, the expression of CTCF returned to normal levels after CR but rebounded in the RE samples. In the pre-B ALL cell line Nalm-6, siRNA-mediated silencing of CTCF expression promoted cell apoptosis and reduced cell proliferation; accordingly, over-expression of a cDNA encoding full-length CTCF protected cells from apoptosis and enhanced cell proliferation. Furthermore, inhibition or activation of the nuclear factor-kappa B (NF-κB) pathway resulted in marked variations in the levels of CTCF mRNA and protein in leukemic cells, indicating that CTCF may be involved downstream of the NF-κB pathway. Moreover, inhibition of the NF-κB pathway increased cell apoptosis, which was partially rescued by ectopic over-expression of CTCF, suggesting that CTCF may play a significant role in the anti-apoptotic pathway mediated by NF-κB. CONCLUSIONS: Our results indicate that CTCF serves as both an anti-apoptotic factor and a proliferative factor in leukemic cells. It potentially contributes to leukemogenesis through the NF-κB pathway in pediatric ALL patients

Drop evaporation on rough hot-spots: effect of wetting modes

Hot-spots are a common occurrence in power electronics which become increasingly hotter as chips become denser. Novel cooling technologies are emerging to cope with this increasing heat load, which imbed a condenser to supply cooling drops to the evaporator resting on the hot-spots. Nonetheless, the evaporation process of the drops has been overlooked. Here, we conducted a series of experiments to understand how the evaporation and motion of drops are influenced by the wetting mode of rough hot-spots. We fabricated three different surfaces exhibiting full (Wenzel) or partial (Cassie–Baxter) wetting and the hot-spot is imposed by laser irradiation. We report a direct link between drop motion and wetting mode with the partial wetting drops being highly mobile, attributable to lower pinning energy based on an energy analysis. This study provides a framework for future modifications in hot-spot cooling to account for drop motion which should greatly influence the overall heat removal performance

Ripk3 signaling regulates HSCs during stress and represses radiation-induced leukemia in mice

Receptor-interacting protein kinase 3 (Ripk3) is one of the critical mediators of inflammatory cytokine-stimulated signaling. Here we show that Ripk3 signaling selectively regulates both the number and the function of hematopoietic stem cells (HSCs) during stress conditions. Ripk3 signaling is not required for normal homeostatic hematopoiesis. However, in response to serial transplantation, inactivation of Ripk3 signaling prevents stress-induced HSC exhaustion and functional HSC attenuation, while in response to fractionated low doses of ionizing radiation (IR), inactivation of Ripk3 signaling accelerates leukemia/lymphoma development. In both situations, Ripk3 signaling is primarily stimulated by tumor necrosis factor-α. Activated Ripk3 signaling promotes the elimination of HSCs during serial transplantation and pre-leukemia stem cells (pre-LSCs) during fractionated IR by inducing Mlkl-dependent necroptosis. Activated Ripk3 signaling also attenuates HSC functioning and represses a pre-LSC-to-LSC transformation by promoting Mlkl-independent senescence. Furthermore, we demonstrate that Ripk3 signaling induces senescence in HSCs and pre-LSCs by attenuating ISR-mediated mitochondrial quality control

LATS kinase-mediated CTCF phosphorylation and selective loss of genomic binding.

Chromatin topological organization is instrumental in gene transcription. Gene-enhancer interactions are accommodated in the same CTCF-mediated insulated neighborhoods. However, it remains poorly understood whether and how the 3D genome architecture is dynamically restructured by external signals. Here, we report that LATS kinases phosphorylated CTCF in the zinc finger (ZF) linkers and disabled its DNA-binding activity. Cellular stress induced LATS nuclear translocation and CTCF ZF linker phosphorylation, and altered the landscape of CTCF genomic binding partly by dissociating it selectively from a small subset of its genomic binding sites. These sites were highly enriched for the boundaries of chromatin domains containing LATS signaling target genes. The stress-induced CTCF phosphorylation and locus-specific dissociation from DNA were LATS-dependent. Loss of CTCF binding disrupted local chromatin domains and down-regulated genes located within them. The study suggests that external signals may rapidly modulate the 3D genome by affecting CTCF genomic binding through ZF linker phosphorylation