Extrinsic properties of automorphism groups of formal groups

We prove two conjectures on the automorphism group of a one-dimensional formal group law defined over a field of positive characteristic. The first is that if a series commutes with a nontorsion automorphism of the formal group law, then that series is already an automorphism. The second is that the group of automorphisms is its own normalizer in the group of all invertible series over the ground field. A consequence of these results is that a formal group law in positive characteristic is determined by any one of its nontorsion automorphisms.Comment: 15 page

Ionization efficiency for nuclear recoils in silicon from ∼50\sim 50 eV to 33 MeV

We present a model for the nuclear recoil ionization efficiency in silicon based on an extension of Lindhard's theory where atomic bond disruption is modeled as a function of the initial ion energy, the interatomic potential, and the average ion-vacancy production energy. A better description of the electronic stopping than the one assumed by Lindhard, the effect of electronic straggling, as well as charge screening and Coulomb repulsion effects of ions are also considered. The model describes the available data over nearly four orders of magnitude in nuclear recoil energy.Comment: 5 pages, 3 figure

The human commensal Bacteroides fragilis binds intestinal mucin

The mammalian gastrointestinal tract harbors a vast microbial ecosystem, known as the microbiota, which benefits host biology. Bacteroides fragilis is an important anaerobic gut commensal of humans that prevents and cures intestinal inflammation. We wished to elucidate aspects of gut colonization employed by B. fragilis. Fluorescence in situ hybridization was performed on colonic tissue sections from B. fragilis and Escherichia coli dual-colonized gnotobiotic mice. Epifluorescence imaging reveals that both E. coli and B. fragilis are found in the lumen of the colon, but only B. fragilis is found in the mucosal layer. This observation suggests that physical association with intestinal mucus could be a possible mechanism of gut colonization by B. fragilis. We investigated this potential interaction using an in vitro mucus binding assay and show here that B. fragilis binds to murine colonic mucus. We further demonstrate that B. fragilis specifically and quantitatively binds to highly purified mucins (the major constituent in intestinal mucus) using flow cytometry analysis of fluorescently labeled purified murine and porcine mucins. These results suggest that interactions between B. fragilis and intestinal mucin may play a critical role during host-bacterial symbiosis

Examining the role of BRICS countries at the global economic and environmental resources nexus

The BRICS countries (Brazil, Russia, India, China and South Africa) are central to future global economic development. However, they are facing both environmental and natural resource stresses due to their rapid economic growth. This study examines the balance between economic benefits and cost of environmental emissions and resource usage in BRICS countries so that future sustainable development insights can be provided. The historical trends of carbon dioxide (CO2), sulfur dioxide (SO2), water, land, energy and material footprints of these countries from 1995 to 2015 are evaluated with a multi-regional input-output model. Also, whether a decoupling relationship exists between economic development, environmental emissions and resources consumption, is examined. In addition, whether environmental emissions and resource usage costs to obtain identical economic gains of these countries in global trade are explored. The major results show that in congruence with economic development, the average annual growth rates of footprint indicators ranged from 0.2% in 1995 to 9.8% in 2015. A decoupling effect did not occur for CO2 emissions or water consumption but did exist for other indicators. Global trade across the supply chain shows to achieve a unit of USD economic benefit from trade, BRICS countries tend to use relatively greater environmental emissions and resource consumption to high income countries, when compared to other income level countries. These emergent economies did receive relatively greater benefits per environmental emissions and resource usage cost from lower-middle and low-income countries

Banach Analytic Sets and a Non-Linear Version of the Levi Extension Theorem

We prove a certain non-linear version of the Levi extension theorem for meromorphic functions. This means that the meromorphic function in question is supposed to be extendable along a sequence of complex curves, which are arbitrary, not necessarily straight lines. Moreover, these curves are not supposed to belong to any finite dimensional analytic family. The conclusion of our theorem is that nevertheless the function in question meromorphically extends along an (infinite dimensional) analytic family of complex curves and its domain of existence is a pinched domain filled in by this analytic family.Comment: 19 pages, This is the final version with significant corrections and improvements. To appear in Arkiv f\"or matemati

How to globalize the circular economy

We call for a global initiative to advance the circular economy. It should be led by the United Nations and involve G20 countries, the World Economic Forum, industry and citizen-oriented organizations. It should gather data, draw lessons, trigger learning and share experiences on how businesses and people use and recycle resources. Policies, missions and incentives should be developed to spread circular-economy practices worldwide

The Placental Interleukin-6 Signaling Controls Fetal Brain Development and Behavior

Epidemiological studies show that maternal immune activation (MIA) during pregnancy is a risk factor for autism. However, mechanisms for how MIA affects brain development and behaviors in offspring remain poorly described. To determine whether placental interleukin-6 (IL-6) signaling is required for mediating MIA on the offspring, we generated mice with restricted deletion of the receptor for IL-6 (IL-6R_) in placental trophoblasts (Cyp19-Cre^(+);Il6ra^(fl/fl)), and tested offspring of Cyp19-Cre^(+);Il6ra^(fl/fl) mothers for immunological, pathological and behavioral abnormalities following induction of MIA. We reveal that MIA results in acute inflammatory responses in the fetal brain. Lack of IL-6 signaling in trophoblasts effectively blocks MIA-induced inflammatory responses in the placenta and the fetal brain. Furthermore, behavioral abnormalities and cerebellar neuropathologies observed in MIA control offspring are prevented in Cyp19-Cre^(+);Il6ra^(fl/fl) offspring. Our results demonstrate that IL-6 activation in placenta is required for relaying inflammatory signals to the fetal brain and impacting behaviors and neuropathologies relevant to neurodevelopmental disease

Specific anchoring modes of two distinct dystrophin rod sub-domains interacting in phospholipid Langmuir films studied by atomic force microscopy and PM-IRRAS.

International audienceDystrophin rod repeats 1-3 sub-domain binds to acidic phosphatidylserine in a small vesicle binding assay, while the repeats 20-24 sub-domain does not. In the present work, we studied the adsorption behaviour of both sub-domains at the air/liquid interface and at the air/lipid interface in a Langmuir trough in order to highlight differences in interfacial properties. The adsorption behaviour of the two proteins at the air/liquid interface shows that they display surface activity while maintaining their alpha-helical secondary structure as shown by PM-IRRAS. Strikingly, R20-24 needs to be highly hydrated even at the interface, while this is not the case for R1-3, indicating that the surface activity is dramatically higher for R1-3 than R20-24. Surface-pressure measurements, atomic force microscopy and PM-IRRAS are used in a Langmuir experiment with DOPC-DOPS monolayers at two different surface pressures, 20mN/m and 30mN/m. At the lower surface pressure, the proteins are adsorbed at the lipid film interface while maintaining its alpha-helical structure. After an increase of the surface pressure, R1-3 subsequently produces a stable film, while R20-24 induces a reorganization of the lipid film with a subsequent decrease of the surface pressure close to the initial value. AFM and PM-IRRAS show that R1-3 is present in high amounts at the interface, being arranged in clusters representing 3.3% of the surface at low pressure. By contrast, R20-24 is present at the interface in small amounts bound only by a few electrostatic residues to the lipid film while the major part of the molecule remains floating in the sub-phase. Then for R1-3, the electrostatic interaction between the proteins and the film is enhanced by hydrophobic interactions. At higher surface pressure, the number of protein clusters increases and becomes closer in both cases implying the electrostatic character of the binding. These results indicate that even if the repeats exhibit large structural similarities, their interfacial properties are highly contrasted by their differential anchor mode in the membrane. Our work provides strong support for distinct physiological roles for the spectrin-like repeats and may partly explain the effects of therapeutic replacement of dystrophin deficiency by minidystrophins

Indigenous Bacteria from the Gut Microbiota Regulate Host Serotonin Biosynthesis

The gastrointestinal (GI) tract contains much of the body’s serotonin (5-hydroxytryptamine, 5-HT), but mechanisms controlling the metabolism of gut-derived 5-HT remain unclear. Here, we demonstrate that the microbiota plays a critical role in regulating host 5-HT. Indigenous spore-forming bacteria (Sp) from the mouse and human microbiota promote 5-HT biosynthesis from colonic enterochromaffin cells (ECs), which supply 5-HT to the mucosa, lumen, and circulating platelets. Importantly, microbiota-dependent effects on gut 5-HT significantly impact host physiology, modulating GI motility and platelet function. We identify select fecal metabolites that are increased by Sp and that elevate 5-HT in chromaffin cell cultures, suggesting direct metabolic signaling of gut microbes to ECs. Furthermore, elevating luminal concentrations of particular microbial metabolites increases colonic and blood 5-HT in germ-free mice. Altogether, these findings demonstrate that Sp are important modulators of host 5-HT and further highlight a key role for host-microbiota interactions in regulating fundamental 5-HT-related biological processes

Modeling an autism risk factor in mice leads to permanent immune dysregulation

Increasing evidence highlights a role for the immune system in the pathogenesis of autism spectrum disorder (ASD), as immune dysregulation is observed in the brain, periphery, and gastrointestinal tract of ASD individuals. Furthermore, maternal infection (maternal immune activation, MIA) is a risk factor for ASD. Modeling this risk factor in mice yields offspring with the cardinal behavioral and neuropathological symptoms of human ASD. In this study, we find that offspring of immune-activated mothers display altered immune profiles and function, characterized by a systemic deficit in CD4^+ TCRβ^+ Foxp3^+ CD25^+ T regulatory cells, increased IL-6 and IL-17 production by CD4^+ T cells, and elevated levels of peripheral Gr-1^+ cells. In addition, hematopoietic stem cells from MIA offspring exhibit altered myeloid lineage potential and differentiation. Interestingly, repopulating irradiated control mice with bone marrow derived from MIA offspring does not confer MIA-related immunological deficits, implicating the peripheral environmental context in long-term programming of immune dysfunction. Furthermore, behaviorally abnormal MIA offspring that have been irradiated and transplanted with immunologically normal bone marrow from either MIA or control offspring no longer exhibit deficits in stereotyped/repetitive and anxiety-like behaviors, suggesting that immune abnormalities in MIA offspring can contribute to ASD-related behaviors. These studies support a link between cellular immune dysregulation and ASD-related behavioral deficits in a mouse model of an autism risk factor