Spatial spread of infectious diseases with conditional vector preferences

We explore the spatial spread of vector-borne infections with conditional vector preferences, meaning that vectors do not visit hosts at random. Vectors may be differentially attracted toward infected and uninfected hosts depending on whether they carry the pathogen or not. The model is expressed as a system of partial differential equations with vector diffusion. We first study the non-spatial model. We show that conditional vector preferences alone (in the absence of any epidemiological feedback on their population dynamics) may result in bistability between the disease-free equilibrium and an endemic equilibrium. A backward bifurcation may allow the disease to persist even though its basic reproductive number is less than one. Bistability can occur only if both infected and uninfected vectors prefer uninfected hosts. Back to the model with diffusion, we show that bistability in the local dynamics may generate travelling waves with either positive or negative spreading speeds, meaning that the disease either invades or retreats into space. In the monostable case, we show that the disease spreading speed depends on the preference of uninfected vectors for infected hosts, but also on the preference of infected vectors for uninfected hosts under some circumstances (when the spreading speed is not linearly determined). We discuss the implications of our results for vector-borne plant diseases, which are the main source of evidence for conditional vector preferences so far.The MODCOV19 CNRS platform, the European Agricultural Fund for Rural Development (EAFRD) within the DPP “Santé & Biodiversité” framework, the DST/NRF SARChI Chair in Mathematical Models and Methods in Biosciences and Bioengineering at the University of Pretoria, South Africa, the Conseil Régional de la Réunion (France), the Conseil Départemental de la Réunion (France), the European Agricultural Fund for Rural Development (EAFRD) and the Centre de Coopération Internationale en Recherche Agronomique pour le Développement (CIRAD), France.https://link.springer.com/journal/2852024-08-03hj2024Mathematics and Applied MathematicsNon

Kinetics of photoinduced ordering in azo-dye films: two-state and diffusion models

We study the kinetics of photoinduced ordering in the azo-dye SD1 photoaligning layers and present the results of modeling performed using two different phenomenological approaches. A phenomenological two state model is deduced from the master equation for an ensemble of two-level molecular systems. Using an alternative approach, we formulate the two-dimensional (2D) diffusion model as the free energy Fokker-Planck equation simplified for the limiting regime of purely in-plane reorientation. The models are employed to interpret the irradiation time dependence of the absorption order parameters extracted from the available experimental data by using the exact solution to the light transmission problem for a biaxially anisotropic absorbing layer. The transient photoinduced structures are found to be biaxially anisotropic whereas the photosteady and the initial states are uniaxial.Comment: revtex4, 34 pages, 9 figure

Parents\u27 Goals: An Analysis of Therapist Reasoning

Purpose: Illustrate the use of DDDM to develop parent-identified goals for occupational therapy and to identify underlying sensory integration factors hypothesized to be impacting participation

Limit theorems for self-similar tilings

We study deviation of ergodic averages for dynamical systems given by self-similar tilings on the plane and in higher dimensions. The main object of our paper is a special family of finitely-additive measures for our systems. An asymptotic formula is given for ergodic integrals in terms of these finitely-additive measures, and, as a corollary, limit theorems are obtained for dynamical systems given by self-similar tilings.Comment: 36 pages; some corrections and improved exposition, especially in Section 4; references adde

Aurora kinase A drives the evolution of resistance to third-generation EGFR inhibitors in lung cancer.

Although targeted therapies often elicit profound initial patient responses, these effects are transient due to residual disease leading to acquired resistance. How tumors transition between drug responsiveness, tolerance and resistance, especially in the absence of preexisting subclones, remains unclear. In epidermal growth factor receptor (EGFR)-mutant lung adenocarcinoma cells, we demonstrate that residual disease and acquired resistance in response to EGFR inhibitors requires Aurora kinase A (AURKA) activity. Nongenetic resistance through the activation of AURKA by its coactivator TPX2 emerges in response to chronic EGFR inhibition where it mitigates drug-induced apoptosis. Aurora kinase inhibitors suppress this adaptive survival program, increasing the magnitude and duration of EGFR inhibitor response in preclinical models. Treatment-induced activation of AURKA is associated with resistance to EGFR inhibitors in vitro, in vivo and in most individuals with EGFR-mutant lung adenocarcinoma. These findings delineate a molecular path whereby drug resistance emerges from drug-tolerant cells and unveils a synthetic lethal strategy for enhancing responses to EGFR inhibitors by suppressing AURKA-driven residual disease and acquired resistance

An Interprofessional, Tailored Behavioral Intervention for Sleep Problems in Autism: Use of Sensory Data to Inform Intervention

Purpose: The purpose of this poster is to demonstrate how Sensory Profile data informed occupational therapy sleep interventions for two participants as part of an Interprofessional Tailored Behavioral Intervention study

Genome-wide association study identifies 30 loci associated with bipolar disorder.

Bipolar disorder is a highly heritable psychiatric disorder. We performed a genome-wide association study (GWAS) including 20,352 cases and 31,358 controls of European descent, with follow-up analysis of 822 variants with P < 1 × 10-4 in an additional 9,412 cases and 137,760 controls. Eight of the 19 variants that were genome-wide significant (P < 5 × 10-8) in the discovery GWAS were not genome-wide significant in the combined analysis, consistent with small effect sizes and limited power but also with genetic heterogeneity. In the combined analysis, 30 loci were genome-wide significant, including 20 newly identified loci. The significant loci contain genes encoding ion channels, neurotransmitter transporters and synaptic components. Pathway analysis revealed nine significantly enriched gene sets, including regulation of insulin secretion and endocannabinoid signaling. Bipolar I disorder is strongly genetically correlated with schizophrenia, driven by psychosis, whereas bipolar II disorder is more strongly correlated with major depressive disorder. These findings address key clinical questions and provide potential biological mechanisms for bipolar disorder