Semisimple types for p -adic classical groups

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On the elliptic nonabelian Fourier transform for unipotent representations of p-adic groups

In this paper, we consider the relation between two nonabelian Fourier transforms. The first one is defined in terms of the Langlands-Kazhdan-Lusztig parameters for unipotent elliptic representations of a split p-adic group and the second is defined in terms of the pseudocoefficients of these representations and Lusztig's nonabelian Fourier transform for characters of finite groups of Lie type. We exemplify this relation in the case of the p-adic group of type G_2.Comment: 17 pages; v2: several minor corrections, references added; v3: corrections in the table with unipotent discrete series of G

Theorie de Lubin-Tate non-abelienne et representations elliptiques

Harris and Taylor proved that the supercuspidal part of the cohomology of the Lubin-Tate tower realizes both the local Langlands and Jacquet-Langlands correspondences, as conjectured by Carayol. Recently, Boyer computed the remaining part of the cohomology and exhibited two defects : first, the representations of GL\_d which appear are of a very particular and restrictive form ; second, the Langlands correspondence is not realized anymore. In this paper, we study the cohomology complex in a suitable equivariant derived category, and show how it encodes Langlands correspondance for all elliptic representations. Then we transfer this result to the Drinfeld tower via an enhancement of a theorem of Faltings due to Fargues. We deduce that Deligne's weight-monodromy conjecture is true for varieties uniformized by Drinfeld's coverings of his symmetric spaces.Comment: 54 page

On a Conjecture of Rapoport and Zink

In their book Rapoport and Zink constructed rigid analytic period spaces $F^{wa}$ for Fontaine's filtered isocrystals, and period morphisms from PEL moduli spaces of $p$-divisible groups to some of these period spaces. They conjectured the existence of an \'etale bijective morphism $F^a \to F^{wa}$ of rigid analytic spaces and of a universal local system of $Q_p$-vector spaces on $F^a$. For Hodge-Tate weights $n-1$ and $n$ we construct in this article an intrinsic Berkovich open subspace $F^0$ of $F^{wa}$ and the universal local system on $F^0$. We conjecture that the rigid-analytic space associated with $F^0$ is the maximal possible $F^a$, and that $F^0$ is connected. We give evidence for these conjectures and we show that for those period spaces possessing PEL period morphisms, $F^0$ equals the image of the period morphism. Then our local system is the rational Tate module of the universal $p$-divisible group and enjoys additional functoriality properties. We show that only in exceptional cases $F^0$ equals all of $F^{wa}$ and when the Shimura group is $GL_n$ we determine all these cases.Comment: v2: 48 pages; many new results added, v3: final version that will appear in Inventiones Mathematica

Australian forested wetlands under climate change:Collapse or proliferation?

Climatically driven perturbations (e.g. intense drought, fire, sea surface temperature rise) can bring ecosystems that are already stressed by long-term climate change and other anthropogenic impacts to a point of collapse. Recent reviews of the responses of Australian ecosystems to climate change and associated stressors have suggested widespread ecosystem collapse is occurring across multiple biomes. Two commonly cited case studies concern forested wetland ecosystems: mangrove forest dieback in northern Australia (2015-16) and riverine forest dieback in the south-east of the continent (2002-09). We present an alternative interpretation that emphasises the dominant signal of climate change effects, rather than the interdecadal signal of climate variability that drives wetland forest dynamics. For both the south-east Australian riverine forests and mangroves of northern Australia, aerial extent remains greater after dieback than in the early 1990s. We interpret dieback and defoliation in both systems as a dry phase response and provide evidence of a current and near-future climate change trajectory of increased areal extent and cover (i.e. tree colonisation and range infilling). In both case studies, climate change-driven increases in tree cover and extent are occurring at the expense of wetland grasslands and the important ecosystem functions they support

Impact of culture towards disaster risk reduction

Number of natural disasters has risen sharply worldwide making the risk of disasters a global concern. These disasters have created significant losses and damages to humans, economy and society. Despite the losses and damages created by disasters, some individuals and communities do not attached much significance to natural disasters. Risk perception towards a disaster not only depends on the danger it could create but also the behaviour of the communities and individuals that is governed by their culture. Within this context, this study examines the relationship between culture and disaster risk reduction (DRR). A comprehensive literature review is used for the study to evaluate culture, its components and to analyse a series of case studies related to disaster risk. It was evident from the study that in some situations, culture has become a factor for the survival of the communities from disasters where as in some situations culture has acted as a barrier for effective DRR activities. The study suggests community based DRR activities as a mechanism to integrate with culture to effectively manage disaster risk

The RNA-Binding Protein Musashi1 Affects Medulloblastoma Growth via a Network of Cancer- Related Genes and Is an Indicator of Poor Prognosis

Musashi1 (Msi1) is a highly conserved RNA-binding protein that is required during the development of the nervous system. Msi1 has been characterized as a stem cell marker, controlling the balance between self-renewal and differentiation, and has also been implicated in tumorigenesis, being highly expressed in multiple tumor types. We analyzed Msi1 expression in a large cohort of medulloblastoma samples and found that Msi1 is highly expressed in tumor tissue compared with normal cerebellum. Notably, high Msi1 expression levels proved to be a sign of poor prognosis. Msi1 expression was determined to be particularly high in molecular subgroups 3 and 4 of medulloblastoma. We determined that Msi1 is required for tumorigenesis because inhibition of Msi1 expression by small-interfering RNAs reduced the growth of Daoy medulloblastoma cells in xenografts. To characterize the participation of Msi1 in medulloblastoma, we conducted different high-throughput analyses. Ribonucleoprotein immunoprecipitation followed by microarray analysis (RIP-chip) was used to identify mRNA species preferentially associated with Msi1 protein in Daoy cells. We also used cluster analysis to identify genes with similar or opposite expression patterns to Msi1 in our medulloblastoma cohort. A network study identified RAC1, CTGF, SDCBP, SRC, PRL, and SHC1 as major nodes of an Msi1-associated network. Our results suggest that Msi1 functions as a regulator of multiple processes in medulloblastoma formation and could become an important therapeutic target

Statistical Inference for Multi-Pathogen Systems

There is growing interest in understanding the nature and consequences of interactions among infectious agents. Pathogen interactions can be operational at different scales, either within a co-infected host or in host populations where they co-circulate, and can be either cooperative or competitive. The detection of interactions among pathogens has typically involved the study of synchrony in the oscillations of the protagonists, but as we show here, phase association provides an unreliable dynamical fingerprint for this task. We assess the capacity of a likelihood-based inference framework to accurately detect and quantify the presence and nature of pathogen interactions on the basis of realistic amounts and kinds of simulated data. We show that when epidemiological and demographic processes are well understood, noisy time series data can contain sufficient information to allow correct inference of interactions in multi-pathogen systems. The inference power is dependent on the strength and time-course of the underlying mechanism: stronger and longer-lasting interactions are more easily and more precisely quantified. We examine the limitations of our approach to stochastic temporal variation, under-reporting, and over-aggregation of data. We propose that likelihood shows promise as a basis for detection and quantification of the effects of pathogen interactions and the determination of their (competitive or cooperative) nature on the basis of population-level time-series data