Data-Driven Analysis of Pareto Set Topology

When and why can evolutionary multi-objective optimization (EMO) algorithms cover the entire Pareto set? That is a major concern for EMO researchers and practitioners. A recent theoretical study revealed that (roughly speaking) if the Pareto set forms a topological simplex (a curved line, a curved triangle, a curved tetrahedron, etc.), then decomposition-based EMO algorithms can cover the entire Pareto set. Usually, we cannot know the true Pareto set and have to estimate its topology by using the population of EMO algorithms during or after the runtime. This paper presents a data-driven approach to analyze the topology of the Pareto set. We give a theory of how to recognize the topology of the Pareto set from data and implement an algorithm to judge whether the true Pareto set may form a topological simplex or not. Numerical experiments show that the proposed method correctly recognizes the topology of high-dimensional Pareto sets within reasonable population size.Comment: 8 pages, accepted at GECCO'18 as a full pape

Produção de sementes de coentro em função dos tipos de adubação.

O objetivo deste trabalho foi avaliar a influência de tipos de adubo na produção de sementes de coentro (Coriandrum sativum L.) nas condições de Botucatu-SP. Utilizou-se sementes Aglofora S.A, cv. Português

Magnetic-Field-Induced Antiferromagnetism in Two-Dimensional Hubbard Model: Analysis of CeRhIn5_5

We propose the mechanism for the magnetic-field-induced antiferromagnetic (AFM) state in a two-dimensional Hubbard model in the vicinity of the AFM quantum critical point (QCP), using the fluctuation-exchange (FLEX) approximation by taking the Zeeman energy due to the magnetic field $B$ into account. In the vicinity of the QCP, we find that the AFM correlation perpendicular to $B$ is enhanced, whereas that parallel to $B$ is reduced. This fact means that the finite magnetic field increases $T_N$, with the AFM order perpendicular to $B$. The increment in $T_N$ can be understood in terms of the reduction of both quantum and thermal fluctuations due to the magnetic field, which is caused by the self-energy effect within the FLEX approximation. The present study naturally explains the increment in $T_N$ in CeRhIn_5 under the magnetic field found recently.Comment: 5 page

Maximal HIV-1 Replication in Alveolar Macrophages during Tuberculosis Requires both Lymphocyte Contact and Cytokines

HIV-1 replication is markedly upregulated in alveolar macrophages (AM) during pulmonary tuberculosis (TB). This is associated with loss of an inhibitory CCAAT enhancer binding protein β (C/EBPβ) transcription factor and activation of nuclear factor (NF)-κB. Since the cellular immune response in pulmonary TB requires lymphocyte–macrophage interaction, a model system was developed in which lymphocytes were added to AM. Contact between lymphocytes and AM reduced inhibitory C/EBPβ, activated NF-κB, and enhanced HIV-1 replication. If contact between lymphocytes and macrophages was prevented, inhibitory C/EBPβ expression was maintained and the HIV-1 long terminal repeat (LTR) was not maximally stimulated although NF-κB was activated. Antibodies that cross-linked macrophage expressed B-7, and vascular cell adhesion molecule and CD40 were used to mimic lymphocyte contact. All three cross-linking antibodies were required to abolish inhibitory C/EBPβ expression. However, the HIV-1 LTR was not maximally stimulated and NF-κB was not activated. Maximal HIV-1–LTR stimulation required both lymphocyte-derived soluble factors, and cross-linking of macrophage expressed costimulatory molecules. High level HIV-1–LTR stimulation was also achieved when IL-1β, IL-6, and TNF-β were added to macrophages with cross-linked costimulatory molecules. Contact between activated lymphocytes and macrophages is necessary to down-regulate inhibitory C/EBPβ, thereby derepressing the HIV-1 LTR. Lymphocyte-derived cytokines activate NF-κB, further enhancing the HIV-1 LTR

PAC1 receptor-mediated clearance of tau in postsynaptic compartments attenuates tau pathology in mouse brain

Accumulation of pathological tau in synapses has been identified as an early event in Alzheimer's disease (AD) and correlates with cognitive decline in patients with AD. Tau is a cytosolic axonal protein, but under disease conditions, tau accumulates in postsynaptic compartments and presynaptic terminals, due to missorting within neurons, transsynaptic transfer between neurons, or a failure of clearance pathways. Using subcellular fractionation of brain tissue from rTg4510 tau transgenic mice with tauopathy and human postmortem brain tissue from patients with AD, we found accumulation of seed-competent tau predominantly in postsynaptic compartments. Tau-mediated toxicity in postsynaptic compartments was exacerbated by impaired proteasome activity detected by measuring lysine-48 polyubiquitination of proteins targeted for proteasomal degradation. To combat the accumulation of tau and proteasome impairment in the postsynaptic compartments of rTg4510 mouse brain, we stimulated the pituitary adenylate cyclase-activating polypeptide (PACAP) type 1 receptor (PAC1R) with its ligand PACAP administered intracerebroventricularly to rTg4510 mice. We observed enhanced synaptic proteasome activity and reduced total tau in postsynaptic compartments in mouse brain after PACAP treatment. The clearance of tau from postsynaptic compartments correlated with attenuated tauopathy and improved cognitive performance of rTg4510 transgenic mice on two behavioral tests. These results suggest that activating PAC1R could prevent accumulation of aggregate-prone tau and indicate a potential therapeutic approach for AD and other tauopathies

The IGF2 intronic miR-483 selectively enhances transcription from IGF2 fetal promoters and enhances tumorigenesis

Insulin-like growth factor 2 (IGF2), a developmentally regulated and maternally imprinted gene, is frequently overexpressed in pediatric cancers. Although loss of imprinting (LOI) at fetal promoters contributes to increased IGF2 in tumors, the magnitude of IGF2 expression suggests the involvement of additional regulatory mechanisms. A microRNA (miRNA) screen of primary Wilms' tumors identified specific overexpression of miR-483-5p, which is embedded within the IGF2 gene. Unexpectedly, the IGF2 mRNA itself is transcriptionally up-regulated by miR-483-5p. A nuclear pool of miR-483-5p binds directly to the 5′ untranslated region (UTR) of fetal IGF2 mRNA, enhancing the association of the RNA helicase DHX9 to the IGF2 transcript and promoting IGF2 transcription. Ectopic expression of miR-483-5p in IGF2-dependent sarcoma cells is correlated with increased tumorigenesis in vivo. Together, these observations suggest a functional positive feedback loop of an intronic miRNA on transcription of its host gene

F-Theory and the Mordell-Weil Group of Elliptically-Fibered Calabi-Yau Threefolds

The Mordell-Weil group of an elliptically fibered Calabi-Yau threefold X contains information about the abelian sector of the six-dimensional theory obtained by compactifying F-theory on X. After examining features of the abelian anomaly coefficient matrix and U(1) charge quantization conditions of general F-theory vacua, we study Calabi-Yau threefolds with Mordell-Weil rank-one as a first step towards understanding the features of the Mordell-Weil group of threefolds in more detail. In particular, we generate an interesting class of F-theory models with U(1) gauge symmetry that have matter with both charges 1 and 2. The anomaly equations --- which relate the Neron-Tate height of a section to intersection numbers between the section and fibral rational curves of the manifold --- serve as an important tool in our analysis.Comment: 29 pages + appendices, 5 figures; v2: minor correction

Different mechanism of two-proton emission from proton-rich nuclei 23^{23}Al and 22^{22}Mg

Two-proton relative momentum ($q_{pp}$) and opening angle ($\theta_{pp}$) distributions from the three-body decay of two excited proton-rich nuclei, namely $^{23}$Al $\rightarrow$ p + p + $^{21}$Na and $^{22}$Mg $\rightarrow$ p + p + $^{20}$Ne, have been measured with the projectile fragment separator (RIPS) at the RIKEN RI Beam Factory. An evident peak at $q_{pp}\sim20$ MeV/c as well as a peak in $\theta_{pp}$ around 30$^\circ$ are seen in the two-proton break-up channel from a highly-excited $^{22}$Mg. In contrast, such peaks are absent for the $^{23}$Al case. It is concluded that the two-proton emission mechanism of excited $^{22}$Mg is quite different from the $^{23}$Al case, with the former having a favorable diproton emission component at a highly excited state and the latter dominated by the sequential decay process