Avi Mayo

The paper develops a mathematical model and formula (HOMA-C) to quantify beta cell carrying capacity in prediabetes, showing significant variation and its association with diabetes risk.

The paper identifies a subset of senescent cells marked by surface ATP6V1B2 that exhibit increased resistance to apoptosis and are associated with DNA repair.

This study identifies five classes of endocrine circuits in humans, revealing shared structural and regulatory principles across 43 hormone systems.

This study quantifies senescence burden at the single-cell level across tissues in mice and human PBMCs, revealing tissue-specific ageing dynamics and senescence marker heterogeneity.

The paper develops a mechanistic model of the HPA axis to explain the cortisol paradox in PTSD, showing that enhanced GR sensitivity leads to low cortisol with normal ACTH and elevated GR activity.

OSDR2.0 infers cell-state transitions and population dynamics from spatial biopsies, improving treatment response prediction in TNBC.

The paper identifies a cold fibrotic network in LUSC TME driven by CAFs and shows its conservation in other CIACs, suggesting therapeutic targets.

The paper examines how subinhibitory concentrations of bacteriostatic and bactericidal antibiotics affect Escherichia coli growth dynamics, revealing distinct temporal responses between the two classes.

The paper presents a theory predicting which longevity interventions compress relative sickspan by steepening the survival curve, supported by evidence from mice, C. elegans, and Drosophila.

The paper models a macrophage-myofibroblast circuit to predict fibrosis types and shows targeting the myofibroblast autocrine loop reduces fibrosis after myocardial infarction.

The paper uses a mathematical model of the HPA axis to show that only CRH-targeting drugs can lower long-term cortisol in mood disorders, while other targets fail due to gland-mass compensation.

This study measures longitudinal cortisol levels in bipolar disorder using hair samples and links cortisol dynamics to mood episodes through mathematical modeling.

This paper designs a synthetic stem-cell circuit in E. coli with biphasic fitness to test a theory about mutation resistance in differentiation, finding it robust to mutations and environmental pressures.

The paper measures antibiotic-mediated bacterial death and finds death rate is linear with growth rate but varies with environmental stress.

This paper models autoimmune disease flares as excitable dynamics, showing how stochastic events trigger relapses and how regulatory cells influence their frequency.

The paper measures damage dynamics in individual E. coli cells under carbon starvation and finds that stochastic noise amplification, not initial conditions, drives lifespan variation, with increasing determinism over time.

The paper analyzes health records to show seasonal patterns in human hormones, finding that effector hormones peak in winter-spring while upstream pituitary hormones peak in summer, suggesting a circannual clock mechanism.

This study identifies a cell-circuit framework for wound healing and fibrosis, revealing three fibrosis outcomes and parameters that control the transition from healing to fibrosis.

The paper investigates the trade-off between precision and economy in gene expression rates and finds that certain rate combinations are missing due to selective pressures.

The paper investigates how evolutionary tradeoffs between multiple tasks shape the genetic polymorphism structure in populations, finding that prevalent polymorphisms align with the Pareto front of phenotypic tradeoffs.

The paper uses dynamic proteomics to study HSV1 infection in individual cells, finding preexisting cell-state differences influence infection outcomes.

This study uses fMRI to show that the lateral occipital complex (LOC) distinguishes human-made from random abstract shapes, correlating with beauty and familiarity ratings.