How long people live depends on their health, and how it changes with age. Individual health can be tracked by the accumulation of age-related health deficits. The fraction of age-related deficits is a simple quantitative measure of human aging. This quantitative frailty index (F) is as good as chronological age in predicting mortality. In this paper, we use a dynamical network model of deficits to explore the effects of interactions between deficits, deficit damage and repair processes, and the connection between the F and mortality. With our model, we qualitatively reproduce Gompertz's law of increasing human mortality with age, the broadening of the F distribution with age, the characteristic nonlinear increase of the F with age, and the increased mortality of high-frailty individuals. No explicit time-dependence in damage or repair rates is needed in our model. Instead, implicit time-dependence arises through deficit interactions-so that the average deficit damage rates increase, and deficit repair rates decrease, with age. We use a simple mortality criterion, where mortality occurs when the most connected node is damaged.

Randomly rotating particles that have been isotropically labeled with rigidly linked fluorophores will undergo non-isotropic (patchy) photobleaching under illumination due to the dipole coupling of fluorophores with light. For a rotational diffusion rate D of the particle and a photobleaching timescale τ of the fluorophores, the dynamics of this process are characterized by the dimensionless combination Dτ . We find significant interparticle fluctuations at intermediate Dτ . These fluctuations vanish at both large and small Dτ , or at small or large elapsed times t. Associated with these fluctuations between particles, we also observe transient non-monotonicities of the brightness of individual particles. These non-monotonicities can be as much 20% of the original brightness. We show that these novel photobleach-fluctuations dominate over variability of single-fluorophore orientation when there are at least 10 3 fluorophores on individual particles.

We have modelled stress concentration around small gaps in anisotropic elastic sheets, corresponding to the peptidoglycan sacculus of bacterial cells, under loading corresponding to the effects of turgor pressure in rod-shaped bacteria. We find that under normal conditions the stress concentration is insufficient to mechanically rupture bacteria, even for gaps up to a micron in length. We then explored the effects of stress-dependent smart-autolysins, as hypothesised by Arthur L Koch [Advances in Microbial Physiology 24, 301 (1983); Research in Microbiology 141, 529 (1990)]. We show that the measured anisotropic elasticity of the PG sacculus can lead to stable circumferential propagation of small gaps in the sacculus. This is consistent with the recent observation of circumferential propagation of PG-associated MreB patches in rod-shaped bacteria. We also find a bistable regime of both circumferential and axial gap propagation, which agrees with behavior reported in cytoskeletal mutants of B. subtilis. We conclude that the elastic anisotropies of a bacterial sacculus, as characterised experimentally, may be relevant for maintaining rod-shaped bacterial growth.