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Local climate conditions play a major role in the biology of the Aedes aegypti mosquito, the main vector responsible for transmitting dengue, zika, chikungunya and yellow fever in urban centers. For this reason, a detailed assessment of periods in which changes in climate conditions affect the number of human cases may improve the timing of vector-control efforts. In this work, we develop new machine-learning algorithms to analyze climate time series and their connection to the occurrence of dengue epidemic years for seven Brazilian state capitals. Our method explores the impact of two key variables—frequency of precipitation and average temperature—during a wide range of time windows in the annual cycle. Our results indicate that each Brazilian state capital considered has its own climate signatures that correlate with the overall number of human dengue-cases. However, for most of the studied cities, the winter preceding an epidemic year shows a strong predictive power. Understanding such climate contributions to the vector’s biology could lead to more accurate prediction models and early warning systems.

The goal of this study was to assess the goodness-of-fit of theoretical models of population dynamics of Aedes aegypti to trap data collected by a long term entomological surveillance program. The carrying capacity K of this vector was estimated at city and neighborhood level. Adult mosquito abundance was measured via adults collected weekly by a network of sticky traps (Mosquitraps) from January 2008 to December 2011 in Vitória, Espírito Santo, Brazil. K was the only free parameter estimated by the model. At the city level, the model with temperature as a driver captured the seasonal pattern of mosquito abundance. At the local level, we observed a spatial heterogeneity in the estimated carrying capacity between neighborhoods, weakly associated with environmental variables related to poor infrastructure. Model goodness-of-fit was influenced by the number of sticky traps, and suggests a minimum of 16 traps at the neighborhood level for surveillance.

We prove limit theorems for systems of interacting diffusions on sparse graphs. For example, we deduce a hydrodynamic limit and the propagation of chaos property for the stochastic Kuramoto model with interactions determined by Erdös-Rényi graphs with constant mean degree. The limiting object is related to a potentially infinite system of SDEs defined over a Galton-Watson tree. Our theorems apply more generally, when the sequence of graphs ("decorated" with edge and vertex parameters) converges in the local weak sense. Our main technical result is a locality estimate bounding the influence of far-away diffusions on one another. We also numerically explore the emergence of synchronization phenomena on Galton-Watson random trees, observing rich phase transitions from synchronized to desynchronized activity among nodes at different distances from the root.

GTPases are molecular switches that regulate a wide range of cellular processes, such as organelle biogenesis, position, shape, and function, vesicular transport between organelles, and signal transduction. These hydrolase enzymes operate by toggling between an active "ON") guanosine triphosphate (GTP)-bound state and an inactive ("OFF") guanosine diphosphate (GDP)-bound state; such a toggle is regulated by GEFs (guanine nucleotide exchange factors) and GAPs (GTPase activating proteins).Here we propose a model for a network motif between monomeric (m) and trimeric (t) GTPases assembled exclusively in eukaryotic cells of multicellular organisms. We develop a system of ordinary differential equations in which these two classes of GT-Pases are interlinked conditional to their ON/OFF states within a motif through coupling and feedback loops. We provide explicit formulae for the steady states of the system and perform classical local stability analysis to systematically investigate the role of the different connections between the GTPase switches. Interestingly, a coupling of the active mGTPase to the GEF of the tGTPase was sufficient to provide two locally stable states: one where both active/inactive forms of the mGTPase can be interpreted as having low concentrations and the other where both m-and tGTPase have high concentrations. Moreover, when a feedback loop from the GEF of the tGTPase to the GAP of the mGTPase was added to the coupled system, two other locally stable states emerged, both having the tGTPase inactivated and being interpreted as having low active tGTPase concentrations. Finally, the addition of a second feedback loop, from the active tGT-Pase to the GAP of the mGTPase, gives rise to a family of steady states that can be parametrized by a range of inactive tGTPase concentrations. Our findings reveal that the coupling of these two different GTPase motifs can dramatically change their steady state behaviors and shed light on how such coupling may impact signaling mechanisms in eukaryotic cells.

The COVID-19 pandemic has had intense, heterogeneous impacts on different communities and geographies in the United States. We explore county-level associations between COVID-19 attributed deaths and social, demographic, vulnerability, and political variables to develop a better understanding of the evolving roles these variables have played in relation to mortality. We focus on the role of political variables, as captured by support for either the Republican or Democratic presidential candidates in the 2020 elections and the stringency of state-wide governor mandates, during three non-overlapping time periods between February 2020 and February 2021. We find that during the first three months of the pandemic, Democratic-leaning and internationally-connected urban counties were affected. During subsequent months (between May and September 2020), Republican counties with high percentages of Hispanic and Black populations were most hardly hit. In the third time period –between October 2020 and February 2021– we find that Republican-leaning counties with loose mask mandates experienced up to 3 times higher death rates than Democratic-leaning counties, even after controlling for multiple social vulnerability factors. Some of these deaths could perhaps have been avoided given that the effectiveness of non-pharmaceutical interventions in preventing uncontrolled disease transmission, such as social distancing and wearing masks indoors, had been well-established at this point in time.

Protein aggregation on the plasma membrane (PM) is of critical importance to many cellular processes such as cell adhesion, endocytosis, fibrillar conformation, and vesicle transport. Lateral diffusion of protein aggregates or clusters on the surface of the PM plays an important role in governing their heterogeneous surface distribution. However, the stability behavior of the surface distribution of protein aggregates remains poorly understood. Therefore, understanding the spatial patterns that can emerge on the PM solely through protein-protein interaction, lateral diffusion, and feedback is an important step towards a complete description of the mechanisms behind protein clustering on the cell surface. In this work, we investigate the pattern formation of a reactiondiffusion model that describes the dynamics of a system of ligand-receptor complexes. The purely diffusive ligand in the cytosol can bind receptors in the PM, and the resultant ligand-receptor complexes not only diffuse laterally but can also form clusters resulting in different oligomers. Finally, the largest oligomers recruit ligands from the cytosol in a positive feedback. From a methodological viewpoint, we provide theoretical estimates for diffusion-driven instabilities of the protein aggregates based on the Turing mechanism. Our main result is a threshold phenomenon, in which a sufficiently high recruitment of ligands promotes the input of new monomeric components and consequently drives the formation of a single-patch spatially heterogeneous steady-state. CONTENTS