Dimension reduction for rotating Bose-Einstein condensates with anisotropic confinement

We consider the three-dimensional time-dependent Gross-Pitaevskii equation arising in the description of rotating Bose-Einstein condensates and study the corresponding scaling limit of strongly anisotropic confinement potentials. The resulting effective equations in one or two spatial dimensions, respectively, are rigorously obtained as special cases of an averaged three dimensional limit model. In the particular case where the rotation axis is not parallel to the strongly confining direction the resulting limiting model(s) include a negative, and thus, purely repulsive quadratic potential, which is not present in the original equation and which can be seen as an effective centrifugal force counteracting the confinement.Comment: 22 page

An effective mass theorem for the bidimensional electron gas in a strong magnetic field

We study the limiting behavior of a singularly perturbed Schr\"odinger-Poisson system describing a 3-dimensional electron gas strongly confined in the vicinity of a plane $(x,y)$ and subject to a strong uniform magnetic field in the plane of the gas. The coupled effects of the confinement and of the magnetic field induce fast oscillations in time that need to be averaged out. We obtain at the limit a system of 2-dimensional Schr\"odinger equations in the plane $(x,y)$, coupled through an effective selfconsistent electrical potential. In the direction perpendicular to the magnetic field, the electron mass is modified by the field, as the result of an averaging of the cyclotron motion. The main tools of the analysis are the adaptation of the second order long-time averaging theory of ODEs to our PDEs context, and the use of a Sobolev scale adapted to the confinement operator

Host Responses to Malassezia spp. in the Mammalian Skin

The skin of mammalian organisms is home for a myriad of microbes. Many of these commensals are thought to have beneficial effects on the host by critically contributing to immune homeostasis. Consequently, dysbiosis can have detrimental effects for the host that may manifest with inflammatory diseases at the barrier tissue. Besides bacteria, fungi make an important contribution to the microbiota and among these, the yeast Malassezia widely dominates in most areas of the skin in healthy individuals. There is accumulating evidence that Malassezia spp. are involved in a variety of skin disorders in humans ranging from non- or mildly inflammatory conditions such as dandruff and pityriasis versicolor to more severe inflammatory skin diseases like seborrheic eczema and atopic dermatitis. In addition, Malassezia is strongly linked to the development of dermatitis and otitis externa in dogs. However, the association of Malassezia spp. with such diseases remains poorly characterized. Until now, studies on the fungus–host interaction remain sparse and they are mostly limited to experiments with isolated host cells in vitro. They suggest a multifaceted crosstalk of Malassezia spp. with the skin by direct activation of the host via conserved pattern recognition receptors and indirectly via the release of fungus-derived metabolites that can modulate the function of hematopoietic and/or non-hematopoietic cells in the barrier tissue. In this review, we discuss our current understanding of the host response to Malassezia spp. in the mammalian skin

Host Immunity to Malassezia in Health and Disease

The microbiota plays an integral role in shaping physical and functional aspects of the skin. While a healthy microbiota contributes to the maintenance of immune homeostasis, dysbiosis can result in the development of diverse skin pathologies. This dichotomous feature of the skin microbiota holds true not only for bacteria, but also for fungi that colonize the skin. As such, the yeast Malassezia, which is by far the most abundant component of the skin mycobiota, is associated with a variety of skin disorders, of which some can be chronic and severe and have a significant impact on the quality of life of those affected. Understanding the causative relationship between Malassezia and the development of such skin disorders requires in-depth knowledge of the mechanism by which the immune system interacts with and responds to the fungus. In this review, we will discuss recent advances in our understanding of the immune response to Malassezia and how the implicated cells and cytokine pathways prevent uncontrolled fungal growth to maintain commensalism in the mammalian skin. We also review how the antifungal response is currently thought to affect the development and severity of inflammatory disorders of the skin and at distant sites

Assessment of immune responses to fungal infections: identification and characterization of immune cells in the infected tissue

The immune system is important to protect the host from fungal infections. Diverse cell types belonging to the innate or adaptive branch of the immune system act in a tightly coordinated and tissue-specific manner. Experimental mouse models of fungal infections have proved essential for assessing the protective principles against different fungal pathogens. Besides pathological, histological, biochemical and molecular parameters, the analysis of phenotypic and functional aspects of immune cells in infected tissues is key for understanding the mechanisms of antifungal defense. In this chapter, we describe a method based on flow cytometry to assess innate and adaptive immune cells isolated from an in vivo context in a qualitative and quantitative manner

Interleukin-17 in Antifungal Immunity

The field of IL-17 biology has received much attention over the last decade owing to the pathogenic role of this cytokine in psoriasis and other autoinflammatory disorders and the successful implementation of IL-17-targeting therapies in patients suffering from these diseases. IL-17-mediated pathologies are contrasted by the important host beneficial effects of this cytokine. IL-17 is essential for regulating microbial colonization in barrier tissues. Rare congenital defects in the IL-17 pathway exemplify the relevance of IL-17 in protective immunity against the opportunistic fungal pathogen C. albicans. However, more recently, evidence is accumulating that IL-17 can also provide protection against fungi other than C. albicans. Importantly, protective IL-17 responses directed against commensal fungi can, under certain conditions, promote inflammation with detrimental consequences for the host, thereby assigning fungi a new role as disease-promoting factors apart from their role as potential infectious agents

IL-17 takes center stage in dermatophytosis

The cytokine IL-17 plays a critical role in host defense against fungal infections. So far, clinical relevance for IL-17 antifungal activity focused on mucocutaneous candidiasis. Burstein and colleagues now provide evidence that type 17 immunity is also essential for defense against dermatophytosis

Averaging of nonlinear Schrödinger equations with strong magnetic confinement

12 pagesInternational audienceWe consider the dynamics of nonlinear Schr\"odinger equations with strong constant magnetic fields. In an asymptotic scaling limit the system exhibits a purely magnetic confinement, based on the spectral properties of the Landau Hamiltonian. Using an averaging technique we derive an associated effective description via an averaged model of nonlinear Schr\"odinger type. In a special case this also yields a derivation of the LLL equation

Role of NS1 and TLR3 in pathogenesis and immunity of WNV

West Nile Virus (WNV) is a mosquito-transmitted flavivirus which causes encephalitis especially in elderly and immunocompromised individuals. Previous studies have suggested the protective role of the Toll-like receptor 3 (TLR3) pathway against WNV entry into the brain, while the WNV non-structural protein 1 (NS1) interferes with the TLR3 signaling pathway, besides being a component of viral genome replication machinery. In this study, we investigated whether immunization with NS1 could protect against WNV neuroinvasion in the context of TLR3 deficiency. We immunized mice with either an intact or deleted TLR3 system (TLR3KO) with WNV envelope glycoprotein (gE) protein, NS1, or a combination of gE and NS1. Immunization with gE or gE/NS1, but not with NS1 alone, induced WNV neutralizing antibodies and protected against WNV brain invasion and inflammation. The presence of intact TLR3 signaling had no apparent effect on WNV brain invasion. However, mock-immunized TLR3KO mice had higher inflammatory cell invasion upon WNV brain infection than NS1-immunized TLR3KO mice and wild type mice. Thus, immunization against NS1 may reduce brain inflammation in a context of TLR3 signaling deficiency