Nature’s light manipulation strategies—in particular those at the origin of bright iridescent colors—have fascinated humans for centuries. In recent decades, insights into the fundamental concepts and physics underlying biological light-matter interactions have enabled a cascade of attempts to copy nature’s optical strategies in synthetic structurally colored materials. However, despite rapid advances in bioinspired materials that emulate and exceed nature’s light manipulation abilities, we tend to create these materials via methods that have little in common with the processes used by biology. In this review, we compare the processes that enable the formation of biological photonic structures with the procedures employed by scientists and engineers to fabricate biologically inspired photonic materials. This comparison allows us to reflect upon the broader strategies employed in synthetic processes and to identify biological strategies which, if incorporated into the human palette of fabrication approaches, could significantly advance our abilities to control material structure in three dimensions across all relevant length scales.

Heart disease remains the leading cause of death globally. Although reperfusion following myocardial ischemia can prevent death by restoring nutrient flow, ischemia/reperfusion injury can cause significant heart damage. The mechanisms that drive ischemia/reperfusion injury are not well understood; currently, few methods can predict the state of the cardiac muscle cell and its metabolic conditions during ischemia. Here, we explored the energetic sustainability of cardiomyocytes, using a model for cellular metabolism to predict the levels of ATP following hypoxia. We modeled glycolytic metabolism with a system of coupled ordinary differential equations describing the individual metabolic reactions within the cardiomyocyte over time. Reduced oxygen levels and ATP consumption rates were simulated to characterize metabolite responses to ischemia. By tracking biochemical species within the cell, our model enables prediction of the cell's condition up to the moment of reperfusion. The simulations revealed a distinct transition between energetically sustainable and unsustainable ATP concentrations for various energetic demands. Our model illustrates how even low oxygen concentrations allow the cell to perform essential functions. We found that the oxygen level required for a sustainable level of ATP increases roughly linearly with the ATP consumption rate. An extracellular O 2 concentration of ϳ0.007 mM could supply basic energy needs in non-beating cardiomyocytes, suggesting that increased collateral circulation may provide an important source of oxygen to sustain the cardiomyocyte during extended ischemia. Our model provides a time-dependent framework for studying various intervention strategies to change the outcome of reperfusion.Globally, ischemic heart disease was the leading cause of death in 2012 and the most rapidly increasing cause of death during 2000 -2012 (1, 2). Ischemia occurs when the circulation of the blood is restricted, thereby limiting the delivery of nutrients and removal of metabolic by-products. The heart can be saved by restoring blood flow using reperfusion techniques such as percutaneous coronary intervention (3). However, even as the heart is saved, reperfusion carries the risk of damaging additional heart tissue. This damage is termed ischemia/reperfusion injury. Various proposals for novel reperfusion techniques have been advanced, but our understanding of ischemia/ reperfusion injury and our ability to mitigate its risk are significantly lacking (4 -9).It is imperative we identify the quantitative conditions that exist in the cardiomyocyte following a period of ischemia. To date, a number of groups have modeled the dynamics of heart tissue (10 -16). However, only Ch'en et al. (10) model ischemic cardiomyocytes as fully deprived of oxygen, and their model does not provide quantitative data of the detailed transition in time between a fully oxygenated myocardium and one that is deficient of oxygen. Wu et al. (17) represent the onset of ischemia from normal conditions (for 30 s). An alternat...

During metamorphosis, the wings of a butterfly sprout hundreds of thousands of scales with intricate microstructures and nano-structures that determine the wings’ optical appearance, wetting characteristics, thermodynamic properties, and aerodynamic behavior. Although the functional characteristics of scales are well known and prove desirable in various applications, the dynamic processes and temporal coordination required to sculpt the scales’ many structural features remain poorly understood. Current knowledge of scale growth is primarily gained from ex vivo studies of fixed scale cells at discrete time points; to fully understand scale formation, it is critical to characterize the time-dependent morphological changes throughout their development. Here, we report the continuous, in vivo, label-free imaging of growing scale cells of Vanessa cardui using speckle-correlation reflection phase microscopy. By capturing time-resolved volumetric tissue data together with nanoscale surface height information, we establish a morphological timeline of wing scale formation and gain quantitative insights into the underlying processes involved in scale cell patterning and growth. We identify early differences in the patterning of cover and ground scales on the young wing and quantify geometrical parameters of growing scale features, which suggest that surface growth is critical to structure formation. Our quantitative, time-resolved in vivo imaging of butterfly scale development provides the foundation for decoding the processes and biomechanical principles involved in the formation of functional structures in biological materials.

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