A Note on Unlinking Numbers of Montesinos Links

Sin resume

Thomas-Ehrman shifts in nuclei around ^{16}O and role of residual nuclear interaction

The asymmetry in the energy spectra between mirror nuclei (the Thomas-Ehrman shifts) around $^{16}$O is investigated from a phenomenological viewpoint. The recent data on proton-rich nuclei indicates that the residual nuclear interaction is reduced for the loosely bound s-orbit by as much as 30%, which originates in the broad radial distribution of the proton single-particle wave function.Comment: to appear in Phys. Lett. B, with 3 eps figure

On the density matrix for the kink ground state of higher spin XXZ chain

The exact expression for the density matrix of the kink ground state of higher spin XXZ chain is obtained

Myosin-II reorganization during mitosis is controlled temporally by its dephosphorylation and spatially by Mid1 in fission yeast

Cytokinesis in many eukaryotes requires an actomyosin contractile ring. Here, we show that in fission yeast the myosin-II heavy chain Myo2 initially accumulates at the division site via its COOH-terminal 134 amino acids independently of F-actin. The COOH-terminal region can access to the division site at early G2, whereas intact Myo2 does so at early mitosis. Ser1444 in the Myo2 COOH-terminal region is a phosphorylation site that is dephosphorylated during early mitosis. Myo2 S1444A prematurely accumulates at the future division site and promotes formation of an F-actin ring even during interphase. The accumulation of Myo2 requires the anillin homologue Mid1 that functions in proper ring placement. Myo2 interacts with Mid1 in cell lysates, and this interaction is inhibited by an S1444D mutation in Myo2. Our results suggest that dephosphorylation of Myo2 liberates the COOH-terminal region from an intramolecular inhibition. Subsequently, dephosphorylated Myo2 is anchored by Mid1 at the medial cortex and promotes the ring assembly in cooperation with F-actin

Reflection equation for the N=3 Cremmer-Gervais R-matrix

We consider the reflection equation of the N=3 Cremmer-Gervais R-matrix. The reflection equation is shown to be equivalent to 38 equations which do not depend on the parameter of the R-matrix, q. Solving those 38 equations. the solution space is found to be the union of two types of spaces, each of which is parametrized by the algebraic variety $\mathbb{P}^1(\mathbb{C}) \times \mathbb{P}^1(\mathbb{C}) \times \mathbb{P}^2(\mathbb{C})$ and $\mathbb{C} \times \mathbb{P}^1(\mathbb{C}) \times \mathbb{P}^2(\mathbb{C})$.Comment: 28 pages, revised versio

Response of bacterioplankton community structure to an artificial gradient of pCO2 in the Arctic Ocean

In order to test the influences of ocean acidification on the ocean pelagic ecosystem, so far the largest CO2 manipulation mesocosm study (European Project on Ocean Acidification, EPOCA) was performed in Kings Bay (Kongsfjorden), Spitsbergen. During a 30 day incubation, bacterial diversity was investigated using DNA fingerprinting and clone library analysis of bacterioplankton samples. Terminal restriction fragment length polymorphism (T-RFLP) analysis of the PCR amplicons of the 16S rRNA genes revealed that general bacterial diversity, taxonomic richness and community structure were influenced by the variation of productivity during the time of incubation, but not the degree of ocean acidification. A BIOENV analysis suggested a complex control of bacterial community structure by various biological and chemical environmental parameters. The maximum apparent diversity of bacterioplankton (i.e., the number of T-RFs) in high and low pCO2 treatments differed significantly. A negative relationship between the relative abundance of Bacteroidetes and pCO2 levels was observed for samples at the end of the experiment by the combination of T-RFLP and clone library analysis. Our study suggests that ocean acidification affects the development of bacterial assemblages and potentially impacts the ecological function of the bacterioplankton in the marine ecosystem

TPXL-1 activates Aurora A to clear contractile ring components from the polar cortex during cytokinesis

During cytokinesis, a signal from the central spindle that forms between the separating anaphase chromosomes promotes the accumulation of contractile ring components at the cell equator, while a signal from the centrosomal microtubule asters inhibits accumulation of contractile ring components at the cell poles. However, the molecular identity of the inhibitory signal has remained unknown. To identify molecular components of the aster-based inhibitory signal, we developed a means to monitor the removal of contractile ring proteins from the polar cortex after anaphase onset. Using this assay, we show that polar clearing is an active process that requires activation of Aurora A kinase by TPXL-1. TPXL-1 concentrates on astral microtubules coincident with polar clearing in anaphase, and its ability to recruit Aurora A and activate its kinase activity are essential for clearing. In summary, our data identify Aurora A kinase as an aster-based inhibitory signal that restricts contractile ring components to the cell equator during cytokinesis.We thank the Caenorhabditis Genetic Center (funded by the National Institutes of Health Office of Research Infrastructure Programs P40 OD010440) for strains. This work was supported by grants to K. Oegema (National Institutes of Health; GM074207), E. Zanin (Deutsche Forschungsgemeinschaft, ZA619/3-1), and A.X. Carvalho (European Research Council; 640553–ACTOMYO). T. Kim was supported by a grant to Arshad Desai (National Institutes of Health; GM074215). K. Oegema receives salary and other support from the Ludwig Institute for Cancer Research. S. Mangal is a member of International Max Planck Research School for Molecular Life Sciences, and J. Sacher is a member of the Life Science Munich graduate program; both thank their programs for support

A unified framework for efficient estimation of general treatment models

Funder: National Natural Science Foundation of China; Id: http://dx.doi.org/10.13039/501100001809Funder: JSPS; Id: http://dx.doi.org/10.13039/501100001691Funder: KAKENHI; Id: http://dx.doi.org/10.13039/501100001691Funder: Natural Science Foundation of ChinaFunder: Renmin University of China; Id: http://dx.doi.org/10.13039/501100004260This paper presents a weighted optimization framework that unifies the binary, multivalued, and continuous treatment—as well as mixture of discrete and continuous treatment—under a unconfounded treatment assignment. With a general loss function, the framework includes the average, quantile, and asymmetric least squares causal effect of treatment as special cases. For this general framework, we first derive the semiparametric efficiency bound for the causal effect of treatment, extending the existing bound results to a wider class of models. We then propose a generalized optimization estimator for the causal effect with weights estimated by solving an expanding set of equations. Under some sufficient conditions, we establish the consistency and asymptotic normality of the proposed estimator of the causal effect and show that the estimator attains the semiparametric efficiency bound, thereby extending the existing literature on efficient estimation of causal effect to a wider class of applications. Finally, we discuss estimation of some causal effect functionals such as the treatment effect curve and the average outcome. To evaluate the finite sample performance of the proposed procedure, we conduct a small‐scale simulation study and find that the proposed estimation has practical value. In an empirical application, we detect a significant causal effect of political advertisements on campaign contributions in the binary treatment model, but not in the continuous treatment model.</jats:p

A Unified Framework for Efficient Estimation of General Treatment Models

This paper presents a weighted optimization framework that unifies the binary, multivalued, continuous, as well as mixture of discrete and continuous treatment, under the unconfounded treatment assignment. With a general loss function, the framework includes the average, quantile and asymmetric least squares causal effect of treatment as special cases. For this general framework, we first derive the semiparametric efficiency bound for the causal effect of treatment, extending the existing bound results to a wider class of models. We then propose a generalized optimization estimation for the causal effect with weights estimated by solving an expanding set of equations. Under some sufficient conditions, we establish consistency and asymptotic normality of the proposed estimator of the causal effect and show that the estimator attains our semiparametric efficiency bound, thereby extending the existing literature on efficient estimation of causal effect to a wider class of applications. Finally, we discuss estimation of some causal effect functionals such as the treatment effect curve and the average outcome. To evaluate the finite sample performance of the proposed procedure, we conduct a small scale simulation study and find that the proposed estimation has practical value. To illustrate the applicability of the procedure, we revisit the literature on campaign advertise and campaign contributions. Unlike the existing procedures which produce mixed results, we find no evidence of campaign advertise on campaign contribution