Microlensing planet detection via geosynchronous and low Earth orbit satellites

Planet detection through microlensing is usually limited by a well-known degeneracy in the Einstein timescale $t_E$, which prevents mass and distance of the lens to be univocally determined. It has been shown that a satellite in geosynchronous orbit could provide masses and distances for most standard planetary events ($t_E \approx 20$ days) via a microlens parallax measurement. This paper extends the analysis to shorter Einstein timescales, $t_E \approx 1$ day, when dealing with the case of Jupiter-mass lenses. We then study the capabilities of a low Earth orbit satellite on even shorter timescales, $t_E \approx 0.1$ days. A Fisher matrix analysis is employed to predict how the 1-$\sigma$ error on parallax depends on $t_E$ and the peak magnification of the microlensing event. It is shown that a geosynchronous satellite could detect parallaxes for Jupiter-mass free floaters and discover planetary systems around very low-mass brown dwarfs. Moreover, a low Earth orbit satellite could lead to the discovery of Earth-mass free-floating planets. Limitations to these results can be the strong requirements on the photometry, the effects of blending, and in the case of the low orbit, the Earth's umbra.Comment: 5 pages, 3 figures. Minor language edits. Accepted for publication in Astronomy & Astrophysic

The Complexity of Admissibility in Omega-Regular Games

Iterated admissibility is a well-known and important concept in classical game theory, e.g. to determine rational behaviors in multi-player matrix games. As recently shown by Berwanger, this concept can be soundly extended to infinite games played on graphs with omega-regular objectives. In this paper, we study the algorithmic properties of this concept for such games. We settle the exact complexity of natural decision problems on the set of strategies that survive iterated elimination of dominated strategies. As a byproduct of our construction, we obtain automata which recognize all the possible outcomes of such strategies

SHACL Satisfiability and Containment

The Shapes Constraint Language (SHACL) is a recent W3C recommendation language for validating RDF data. Specifically, SHACL documents are collections of constraints that enforce particular shapes on an RDF graph. Previous work on the topic has provided theoretical and practical results for the validation problem, but did not consider the standard decision problems of satisfiability and containment, which are crucial for verifying the feasibility of the constraints and important for design and optimization purposes. In this paper, we undertake a thorough study of the different features of SHACL by providing a translation to a new first-order language, called, that precisely captures the semantics of SHACL w.r.t. satisfiability and containment. We study the interaction of SHACL features in this logic and provide the detailed map of decidability and complexity results of the aforementioned decision problems for different SHACL sublanguages. Notably, we prove that both problems are undecidable for the full language, but we present decidable combinations of interesting features

A kinetic BGK edge-based scheme including vibrational and electronic energy modes for high-Mach flows

A first principles formulation for the calorically imperfect behavior of gases is here proposed within a Boltzmann-type discretisation of the Navier–Stokes equations. The formulation is intended to enhance the consistency of gas kinetic schemes (GKS) with the physics of supersonic and hypersonic regimes where vibrational and electronic energy modes are activated before any thermal nonequilibrium or chemical activity takes place. The so-called node-pair BGK scheme, an edge-based implementation of the GKS, is considered in the present work for the implementation of a thermodynamic model where the calorically imperfect behavior is obtained from a modification of the way the different moments of the particle distribution function are computed and eventually used to determine the fluxes of conserved quantities across the boundary of each control volume. The method is validated on a series of canonical test cases for supersonic and hypersonic flows

Viral expression and molecular profiling in liver tissue versus microdissected hepatocytes in hepatitis B virus - associated hepatocellular carcinoma.

Background: The molecular mechanisms whereby hepatitis B virus (HBV) induces hepatocellular carcinoma (HCC) remain elusive. We used genomic and molecular techniques to investigate host-virus interactions by studying multiple areas of the same liver from patients with HCC. Methods: We compared the gene signature of whole liver tissue (WLT) versus laser capture-microdissected (LCM) hepatocytes along with the intrahepatic expression of HBV. Gene expression profiling was performed on up to 17 WLT specimens obtained at various distances from the tumor center from individual livers of 11 patients with HCC and on selected LCM samples. HBV markers in liver and serum were determined by real-time polymerase chain reaction (PCR)and confocal immunofluorescence. Results: Analysis of 5 areas of the liver showed a sharp change in gene expression between the immediate perilesional area and tumor periphery that correlated with a significant decrease in the intrahepatic expression of HB surface antigen (HBsAg). The tumor was characterized by a large preponderance of down-regulated genes, mostly involved in the metabolism of lipids and fatty acids, glucose, amino acids and drugs, with down-regulation of pathways involved in the activation of PXR/RXR and PPARα/RXRα nuclear receptors, comprising PGC-1α and FOXO1, two key regulators critically involved not only in the metabolic functions of the liver but also in the life cycle of HBV, acting as essential transcription factors for viral gene expression. These findings were confirmed by gene expression of microdissected hepatocytes. Moreover, LCM of malignant hepatocytes also revealed up-regulation of unique genes associated with cancer and signaling Pathways, including two novel HCC-associated cancer testis antigen genes, NUF2 and TTK. Conclusions: Integrated gene expression profiling of whole liver tissue with that of microdissected hepatocytes demonstrated that HBV-associated HCC is characterized by a metabolism switch-off and by a significant reduction in HBsAg. LCM proved to be a critical tool to validate gene signatures associated with HCC and to identify genes that may play a role in hepatocarcinogenesis, opening new perspectives for the discovery of novel diagnostic markers and therapeutic targets

Human albumin enhances the pathogenic potential of Candida glabrata on vaginal epithelial cells

Funding: M.P., H.H., T.G., and B.H. received funding from the European Union Horizon 2020 research and innovation program under the Marie Sklodowska-Curie grant agreement No 642095 (OPATHY). A.K. and B. H. received support from the European Union Horizon 2020 research and innovation program under the Marie Sklodowska-Curie grant agreement No 812969 (FunHoMic). S.A. and B.H. were supported by funding from the European Union's Horizon 2020 research and innovation program under grant agreement No 847507 (HDM-FUN). B.H. is further supported by the DFG within the Collaborative Research Centre (CRC)/Transregio (TRR) 124 “FungiNet” project C1 (DFG project number 210879364) and the Balance of the Microverse Cluster (Germany´s Excellence Strategy – EXC 2051 – Project-ID 390713860). M.S.G. was supported by the German Research Foundation (Deutsche Forschungsgemeinschaft - DFG) Emmy Noether Program (project no. 434385622 / GR 5617/1-1), and a Research Grant 2019 from the European Society of Clinical Microbiology and Infectious Diseases (ESCMID). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. M.P. and H.H. received salary from grant agreement No 642095 (OPATHY) (2016-2019). A.K. received salary from grant agreement No 812969 (FunHoMic) (2019-2022).Peer reviewedPublisher PD

Social brain, social dysfunction and social withdrawal

The human social brain is complex. Current knowledge fails to define the neurobiological processes underlying social behaviour involving the (patho-) physiological mechanisms that link system-level phenomena to the multiple hierarchies of brain function. Unfortunately, such a high complexity may also be associated with a high susceptibility to several pathogenic interventions. Consistently, social deficits sometimes represent the first signs of a number of neuropsychiatric disorders including schizophrenia (SCZ), Alzheimer's disease (AD) and major depressive disorder (MDD) which leads to a progressive social dysfunction. In the present review we summarize present knowledge linking neurobiological substrates sustaining social functioning, social dysfunction and social withdrawal in major psychiatric disorders. Interestingly, AD, SCZ, and MDD affect the social brain in similar ways. Thus, social dysfunction and its most evident clinical expression (i.e., social withdrawal) may represent an innovative transdiagnostic domain, with the potential of being an independent entity in terms of biological roots, with the perspective of targeted interventions

A New Phenotype in Candida-Epithelial Cell Interaction Distinguishes Colonization- versus Vulvovaginal Candidiasis-Associated Strains

Vulvovaginal candidiasis (VVC) affects nearly 3/4 of women during their lifetime, and its symptoms seriously reduce quality of life. Although Candida albicans is a common commensal, it is unknown if VVC results from a switch from a commensal to pathogenic state, if only some strains can cause VVC, and/or if there is displacement of commensal strains with more pathogenic strains. We studied a set of VVC and colonizing C. albicans strains to identify consistent in vitro phenotypes associated with one group or the other. We find that the strains do not differ in overall genetic profile or behavior in culture media (i.e., multilocus sequence type [MLST] profile, rate of growth, and filamentation), but they show strikingly different behaviors during their interactions with vaginal epithelial cells. Epithelial infections with VVC-derived strains yielded stronger fungal proliferation and shedding of fungi and epithelial cells. Transcriptome sequencing (RNA-seq) analysis of representative epithelial cell infections with selected pathogenic or commensal isolates identified several differentially activated epithelial signaling pathways, including the integrin, ferroptosis, and type I interferon pathways; the latter has been implicated in damage protection. Strikingly, inhibition of type I interferon signaling selectively increases fungal shedding of strains in the colonizing cohort, suggesting that increased shedding correlates with lower interferon pathway activation. These data suggest that VVC strains may intrinsically have enhanced pathogenic potential via differential elicitation of epithelial responses, including the type I interferon pathway. Therefore, it may eventually be possible to evaluate pathogenic potential in vitro to refine VVC diagnosis. IMPORTANCE Despite a high incidence of VVC, we still have a poor understanding of this female-specific disease whose negative impact on women's quality of life has become a public health issue. It is not yet possible to determine by genotype or laboratory phenotype if a given Candida albicans strain is more or less likely to cause VVC. Here, we show that Candida strains causing VVC induce more fungal shedding from epithelial cells than strains from healthy women. This effect is also accompanied by increased epithelial cell detachment and differential activation of the type I interferon pathway. These distinguishing phenotypes suggest it may be possible to evaluate the VVC pathogenic potential of fungal isolates. This would permit more targeted antifungal treatments to spare commensals and could allow for displacement of pathogenic strains with nonpathogenic colonizers. We expect these new assays to provide a more targeted tool for identifying fungal virulence factors and epithelial responses that control fungal vaginitis

Magnetic Field Amplification in Galaxy Clusters and its Simulation

We review the present theoretical and numerical understanding of magnetic field amplification in cosmic large-scale structure, on length scales of galaxy clusters and beyond. Structure formation drives compression and turbulence, which amplify tiny magnetic seed fields to the microGauss values that are observed in the intracluster medium. This process is intimately connected to the properties of turbulence and the microphysics of the intra-cluster medium. Additional roles are played by merger induced shocks that sweep through the intra-cluster medium and motions induced by sloshing cool cores. The accurate simulation of magnetic field amplification in clusters still poses a serious challenge for simulations of cosmological structure formation. We review the current literature on cosmological simulations that include magnetic fields and outline theoretical as well as numerical challenges.Comment: 60 pages, 19 Figure