186 research outputs found

    A remark on the Hard Lefschetz Theorem for K\"ahler orbifolds

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    We give a proof of the hard Lefschetz theorem for orbifolds that does not involve intersection homology. This answers a question of Fulton. We use a foliated version of the hard Lefschetz theorem due to El Kacimi

    Foliations modeling nonrational simplicial toric varieties

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    We establish a correspondence between simplicial fans, not necessarily rational, and certain foliated compact complex manifolds called LVMB-manifolds. In the rational case, Meersseman and Verjovsky have shown that the leaf space is the usual toric variety. We compute the basic Betti numbers of the foliation for shellable fans. When the fan is in particular polytopal, we prove that the basic cohomology of the foliation is generated in degree two. We give evidence that the rich interplay between convex and algebraic geometries embodied by toric varieties carries over to our nonrational construction. In fact, our approach unifies rational and nonrational cases.Comment: 24 pages, 4 figures, expository changes, references updated. Link to the journal http://j.mp/BatZaf; Int. Math. Res. Not. 2015 (Published online February 24, 2015

    Holomorphic Functions on Bundles Over Annuli

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    We consider a family E_m(D,M) of holomorphic bundles constructed as follows: to any given M in GL_n(Z), we associate a "multiplicative automorphism" f of (C*)^n. Now let D be a f-invariant Stein Reinhardt domain in (C*)^n. Then E_m(D,M) is defined as the flat bundle over the annulus of modulus m>0, with fiber D, and monodromy f. We show that the function theory on E_m(D,M) depends nontrivially on the parameters m, M and D. Our main result is that E_m(D,M) is Stein if and only if m log(r(M)) <= 2 \pi^2, where r(M) denotes the max of the spectral radii of M and its inverse. As corollaries, we: -- obtain a classification result for Reinhardt domains in all dimensions; -- establish a similarity between two known counterexamples to a question of J.-P. Serre; -- suggest a potential reformulation of a disproved conjecture of Siu Y.-T

    Pseudoconvex domains spread over complex homogeneous manifolds

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    Using the concept of inner integral curves defined by Hirschowitz we generalize a recent result by Kim, Levenberg and Yamaguchi concerning the obstruction of a pseudoconvex domain spread over a complex homogeneous manifold to be Stein. This is then applied to study the holomorphic reduction of pseudoconvex complex homogeneous manifolds X=G/H. Under the assumption that G is solvable or reductive we prove that X is the total space of a G-equivariant holomorphic fiber bundle over a Stein manifold such that all holomorphic functions on the fiber are constant.Comment: 21 page

    Are social networking sites information sources? Informational purposes of high-school students in using SNSs

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    Although social networking sites such as Facebook or Twitter are widely used by teenagers, to date, research has focused on their social uses. This research sought to investigate the ways in which high school students (15–19 years) use such sites in order to find information. It highlights the importance of considering how young people may use social networking sites for everyday life information as well as for academic and school-oriented information. Findings from a web-based survey of students from the UK, France, Thailand and Denmark show that social networking sites are information sources for most teenagers, especially for information related to social activities. Although academic information seeking was not among the most common reasons for using them, the findings indicate that they are used by many students for such purposes, as well as for everyday life information seeking

    Lung adenocarcinoma originates from retrovirus infection of proliferating type 2 pneumocytes during pulmonary post-natal development or tissue repair

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    Jaagsiekte sheep retrovirus (JSRV) is a unique oncogenic virus with distinctive biological properties. JSRV is the only virus causing a naturally occurring lung cancer (ovine pulmonary adenocarcinoma, OPA) and possessing a major structural protein that functions as a dominant oncoprotein. Lung cancer is the major cause of death among cancer patients. OPA can be an extremely useful animal model in order to identify the cells originating lung adenocarcinoma and to study the early events of pulmonary carcinogenesis. In this study, we demonstrated that lung adenocarcinoma in sheep originates from infection and transformation of proliferating type 2 pneumocytes (termed here lung alveolar proliferating cells, LAPCs). We excluded that OPA originates from a bronchioalveolar stem cell, or from mature post-mitotic type 2 pneumocytes or from either proliferating or non-proliferating Clara cells. We show that young animals possess abundant LAPCs and are highly susceptible to JSRV infection and transformation. On the contrary, healthy adult sheep, which are normally resistant to experimental OPA induction, exhibit a relatively low number of LAPCs and are resistant to JSRV infection of the respiratory epithelium. Importantly, induction of lung injury increased dramatically the number of LAPCs in adult sheep and rendered these animals fully susceptible to JSRV infection and transformation. Furthermore, we show that JSRV preferentially infects actively dividing cell in vitro. Overall, our study provides unique insights into pulmonary biology and carcinogenesis and suggests that JSRV and its host have reached an evolutionary equilibrium in which productive infection (and transformation) can occur only in cells that are scarce for most of the lifespan of the sheep. Our data also indicate that, at least in this model, inflammation can predispose to retroviral infection and cancer

    Klf15 Is Critical for the Development and Differentiation of Drosophila Nephrocytes

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    Insect nephrocytes are highly endocytic scavenger cells that represent the only invertebrate model for the study of human kidney podocytes. Despite their importance, nephrocyte development is largely uncharacterised. This work tested whether the insect ortholog of mammalian Kidney Krüppel-Like Factor (Klf15), a transcription factor required for mammalian podocyte differentiation, was required for insect nephrocyte development. It was found that expression of Drosophila Klf15 (dKlf15, previously known as Bteb2) was restricted to the only two nephrocyte populations in Drosophila, the garland cells and pericardial nephrocytes. Loss of dKlf15 function led to attrition of both nephrocyte populations and sensitised larvae to the xenotoxin silver nitrate. Although pericardial nephrocytes in dKlf15 loss of function mutants were specified during embryogenesis, they failed to express the slit diaphragm gene sticks and stones and did not form slit diaphragms. Conditional silencing of dKlf15 in adults led to reduced surface expression of the endocytic receptor Amnionless and loss of in vivo scavenger function. Over-expression of dKlf15 increased nephrocyte numbers and rescued age-dependent decline in nephrocyte function. The data place dKlf15 upstream of sns and Amnionless in a nephrocyte-restricted differentiation pathway and suggest dKlf15 expression is both necessary and sufficient to sustain nephrocyte differentiation. These findings explain the physiological relevance of dKlf15 in Drosophila and imply that the role of KLF15 in human podocytes is evolutionarily conserve

    A roadmap for the Human Developmental Cell Atlas

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    The Human Developmental Cell Atlas (HDCA) initiative, which is part of the Human Cell Atlas, aims to create a comprehensive reference map of cells during development. This will be critical to understanding normal organogenesis, the effect of mutations, environmental factors and infectious agents on human development, congenital and childhood disorders, and the cellular basis of ageing, cancer and regenerative medicine. Here we outline the HDCA initiative and the challenges of mapping and modelling human development using state-of-the-art technologies to create a reference atlas across gestation. Similar to the Human Genome Project, the HDCA will integrate the output from a growing community of scientists who are mapping human development into a unified atlas. We describe the early milestones that have been achieved and the use of human stem-cell-derived cultures, organoids and animal models to inform the HDCA, especially for prenatal tissues that are hard to acquire. Finally, we provide a roadmap towards a complete atlas of human development

    A Splice Isoform of DNedd4, DNedd4-Long, Negatively Regulates Neuromuscular Synaptogenesis and Viability in Drosophila

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    Neuromuscular (NM) synaptogenesis is a tightly regulated process. We previously showed that in flies, Drosophila Nedd4 (dNedd4/dNedd4S) is required for proper NM synaptogenesis by promoting endocytosis of commissureless from the muscle surface, a pre-requisite step for muscle innervation. DNedd4 is an E3 ubiquitin ligase comprised of a C2-WW(x3)-Hect domain architecture, which includes several splice isoforms, the most prominent ones are dNedd4-short (dNedd4S) and dNedd4-long (dNedd4Lo).We show here that while dNedd4S is essential for NM synaptogenesis, the dNedd4Lo isoform inhibits this process and causes lethality. Our results reveal that unlike dNedd4S, dNedd4Lo cannot rescue the lethality of dNedd4 null (DNedd4(T121FS)) flies. Moreover, overexpression of UAS-dNedd4Lo specifically in wildtype muscles leads to NM synaptogenesis defects, impaired locomotion and larval lethality. These negative effects of dNedd4Lo are ameliorated by deletion of two regions (N-terminus and Middle region) unique to this isoform, and by inactivating the catalytic activity of dNedd4Lo, suggesting that these unique regions, as well as catalytic activity, are responsible for the inhibitory effects of dNedd4Lo on synaptogenesis. In accord with these findings, we demonstrate by sqRT-PCR an increase in dNedd4S expression relative to the expression of dNedd4Lo during embryonic stages when synaptogenesis takes place.Our studies demonstrate that splice isoforms of the same dNedd4 gene can lead to opposite effects on NM synaptogenesis
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