Questions and conjectures about the modular representation theory of the general linear group GLn(F2) and the Poincar\'e series of unstable modules

This note is devoted to some questions about the representation theory over the finite field $\mathbb{F}_2$ of the general linear groups $\mathbb{GL_n(F_2)}$ and Poincar\'e series of unstable modules. The first draft was describing two conjectures. They were presented during talks made at VIASM in summer 2013. Since then one conjecture has been disproved, the other one has been proved. These results naturally lead to new questions which are going to be discussed. In winter 2013, Nguyen Dang Ho Hai proved the second conjecture, he disproved the first one in spring 2014. Up to now, the proof of the second one depends on a major topological result: the Segal conjecture. This discussion could be extended to an odd prime, but we will not do it here, just a small number of remarks will be made

LANNES' T FUNCTOR ON INJECTIVE UNSTABLE MODULES AND HARISH-CHANDRA RESTRICTION

In the 1980's, the magic properties of the cohomology of elementary abelian groups as modules over the Steenrod algebra initiated a long lasting interaction between topology and modular representation theory in natural characteristic. The Adams-Gunawardena-Miller theorem in particular, showed that their decomposition is governed by the modular representations of the semi-groups of square matrices. Applying Lannes' T functor on the summands L P := Hom Mn(Fp) (P, H * (F p) n) defines an intriguing construction in representation theory. We show that T(L P) ∼ = L P ⊕ H * V 1 ⊗ L δ(P) , defining a functor δ from F p [M n (F p)]-projectives to F p [M n−1 (F p)]-projectives. We relate this new functor δ to classical constructions in the representation theory of the general linear groups

Software-Defined Network-Based Vehicular Networks: A Position Paper on Their Modeling and Implementation

There is a strong devotion in the automotive industry to be part of a wider progression towards the Fifth Generation (5G) era. In-vehicle integration costs between cellular and vehicle-to-vehicle networks using Dedicated Short Range Communication could be avoided by adopting Cellular Vehicle-to-Everything (C-V2X) technology with the possibility to re-use the existing mobile network infrastructure. More and more, with the emergence of Software Defined Networks, the flexibility and the programmability of the network have not only impacted the design of new vehicular network architectures but also the implementation of V2X services in future intelligent transportation systems. In this paper, we define the concepts that help evaluate software-defined-based vehicular network systems in the literature based on their modeling and implementation schemes. We first overview the current studies available in the literature on C-V2X technology in support of V2X applications. We then present the different architectures and their underlying system models for LTE-V2X communications. We later describe the key ideas of software-defined networks and their concepts for V2X services. Lastly, we provide a comparative analysis of existing SDN-based vehicular network system grouped according to their modeling and simulation concepts. We provide a discussion and highlight vehicular ad-hoc networks' challenges handled by SDN-based vehicular networks.Comment: 14 pages, 3 figures, Sensors 201

Type I IFNs and TNF cooperatively reprogram the macrophage epigenome to promote inflammatory activation

Cross-regulation of Toll-like receptor responses by cytokines is essential for effective host defense, avoidance of toxicity, and homeostasis, but the underlying mechanisms are not well understood. A comprehensive epigenomic approach in human macrophages showed that the proinflammatory cytokines TNF and type I IFNs induce transcriptional cascades that alter chromatin states to broadly reprogram TLR4-induced responses. TNF tolerized inflammatory genes to prevent toxicity, while preserving antiviral and metabolic gene induction. Type I IFNs potentiated TNF inflammatory function by priming chromatin to prevent silencing of inflammatory NF-κB target genes. Priming of chromatin enabled robust transcriptional responses to weak upstream signals. Similar chromatin regulation occurred in human diseases. Our findings reveal that signaling crosstalk between IFNs and TNF is integrated at the level of chromatin to reprogram inflammatory responses, and identify new functions and mechanisms of action of these cytokines

Impact of UV-H₂O₂ advanced oxidation and aging processes on GAC capacity for the removal of cyanobacterial taste and odor compounds

ABSTRACT: Cyanobacteria and their taste and odor (T&O) compounds are a growing concern in water sources globally. Geosmin and 2-methylisoborneol (MIB) are the most commonly detected T&O compounds associated with cyanobacterial presence in drinking water sources. The use of ultraviolet and hydrogen peroxide (H₂O₂) as an advanced oxidation treatment for T&O control is an emerging technology. However, residual H₂O₂ (>80% of the initial dose) has to be removed from water prior final disinfection. Recently, granular activated carbon (GAC) is used to remove H₂O₂ residual. The objective of this study is to assess the impact of H₂O₂ quenching and aging processes on GAC capacity for the removal of geosmin and MIB. Pilot columns with different types of GAC and presence/absence of H₂O₂ have been used for this study. H₂O₂ removal for the operational period of 6 months has no significant impact on GAC capacity to remove the geosmin and MIB from water

The role of AdipoR1 and AdipoR2 in liver fibrosis

Activation of the adiponectin (APN) signaling axis retards liver fibrosis. However, understanding of the role of AdipoR1 and AdipoR2 in mediating this response is still rudimentary. Here, we sought to elucidate the APN receptor responsible for limiting liver fibrosis by employing AdipoR1 and AdipoR2 knock-out mice in the carbon tetrachloride (CCl4) model of liver fibrosis. In addition, we knocked down receptor function in primary hepatic stellate cells (HSCs) in vitro. Following the development of fibrosis, AdipoR1 and AdipoR2 KO mice had no quantitative difference in fibrosis by Sirius red staining. However, AdipoR2 KO mice had an enhanced fibrotic signature with increased Col1-α1, TGFß-1, TIMP-1, IL-10, MMP-2 and MMP-9. Knockdown of AdipoR1 or AdipoR2 in HSCs followed by APN treatment demonstrated that AdipoR1 and AdipoR2 did not affect proliferation or TIMP-1 gene expression, while AdipoR2 modulated Col1-α1 and α-SMA gene expression, HSC migration, and AMPK activity. These finding suggest that AdipoR2 is the major APN receptor on HSCs responsible for mediating its anti-fibrotic effects

Identification and assessment of water quality risks associated with sludge supernatant recycling in the presence of cyanobacteria.

This study focussed on the fate of cyanobacteria cells and associated metabolites during the sludge management processes that follow the conventional drinking water treatment train. The topic is of importance, as the release of metabolites during sludge treatment may pose a risk to water quality if supernatant is recycled to the head of the plant. The study of the kinetics of cell damage and metabolite release into the supernatant is complicated by simultaneous and rapid natural removal processes. In this study, the release of organic material from cyanobacterial sludge was monitored simultaneously with secondary metabolites (Microcystins (MCs), cylindrosperopsin (CYN), and geosmin (GSM)) as an additional parameter to aid in understanding the range of processes occurring in sludge. Only GSM produced by Dolichospermum circinale was found to represent a low risk, as the compound is readily degraded. In contrast, the metabolites CYN and MC were shown to increase in concentration during simulated sludge treatment, suggesting that this could occur within full scale sludge treatment facilities with a range of cyanobacteria species, metabolites and water quality. A generic risk matrix was developed, incorporating the type of cyanobacteria, metabolite production, and the treatment

Targeting mTOR and Src restricts hepatocellular carcinoma growth in a novel murine liver cancer model

Liver cancer is a poor prognosis cancer with limited treatment options. To develop a new therapeutic approach, we derived HCC cells from a known model of murine hepatocellular carcinoma (HCC). We treated adiponectin (APN) knock-out mice with the carcinogen diethylnitrosamine, and the resulting tumors were 7-fold larger than wild-type controls. Tumors were disassociated from both genotypes and their growth characteristics evaluated. A52 cells from APN KO mice had the most robust growth in vitro and in vivo, and presented with pathology similar to the parental tumor. All primary tumors and cell lines exhibited activity of the mammalian target of Rapamycin (mTOR) and Src pathways. Subsequent combinatorial treatment, with the mTOR inhibitor Rapamycin and the Src inhibitor Dasatinib reduced A52 HCC growth 29-fold in vivo. Through protein and histological analyzes we observed activation of these pathways in human HCC, suggesting that targeting both mTOR and Src may be a novel approach for the treatment of HCC