Engineering structures are often subjected to the conditions of cyclic-loading, which onsets material fatigue, detrimentally affecting the service-life and damage tolerance of components and joints. Carbon fibre reinforced plastics (CFRP) are high-strength, lowweight composites that are gaining ubiquity in place of metals and glass fibre reinforced plastics (GFRP) not only due to their outstanding strength-to-weight properties, but also because carbon fibres are relatively inert to environmental degradation and as such, show potential as corrosion resistant materials. The effects of cyclic loading on the fatigue of CFRP are detailed in several papers. As such, collating research on CFRP fatigue into a single document is a worthwhile exercise, as it will benefit the engineering-readership interested in designing fatigue resistant structures and components using CFRP. This review article aims to provide the most relevant and up-to-date information on the fatigue of CFRP. The review focuses in particular on defining fatigue and the mechanics of cyclically-loaded composites, elucidating the fatigue response and fatigue properties of CFRP in different forms, discussing the importance of environmental factors on the fatigue performance and service-life, and summarising the different approaches taken to modelling fatigue in CFRP.

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SummaryKeratin intermediate filament (IF) proteins are epithelial cell cytoskeletal components that provide structural stability and protection from cell stress, among other cellular and tissue-specific functions. Numerous human diseases are associated with IF gene mutations, but the function of keratins in the endocrine pancreas and their potential significance for glycaemic control are unknown. The impact of keratins on b-cell organisation and systemic glucose control was assessed using keratin 8 (K8) wild-type (K8 +/+ ) and K8 knockout (K8 2/2 ) mice. Islet b-cell keratins were characterised under basal conditions, in streptozotocin (STZ)-induced diabetes and in non-obese diabetic (NOD) mice. STZ-induced diabetes incidence and islet damage was assessed in K8 +/+ and K8 2/2 mice. K8 and K18 were the predominant keratins in islet b-cells and K82/2 mice expressed only remnant K18 and K7. K8 deletion resulted in lower fasting glucose levels, increased glucose tolerance and insulin sensitivity, reduced glucose-stimulated insulin secretion and decreased pancreatic insulin content. GLUT2 localisation and insulin vesicle morphology were disrupted in K8 2/2 b-cells. The increased levels of cytoplasmic GLUT2 correlated with resistance to high-dose STZ-induced injury in K8 2/2 mice. However, K8 deletion conferred no long-term protection from STZ-induced diabetes and prolonged STZ-induced stress caused increased exocrine damage in K8 2/2 mice. b-cell keratin upregulation occurred 2 weeks after treatments with low-dose STZ in K8 +/+ mice and in diabetic NOD mice, suggesting a role for keratins, particularly in non-acute islet stress responses. These results demonstrate previously unrecognised functions for keratins in b-cell intracellular organisation, as well as for systemic blood glucose control under basal conditions and in diabetes-induced stress.

The measurement and understanding of collective solvation dynamics in DNA have vital biological implications, as protein and ligand binding to DNA can be directly controlled by complex electrostatic interactions of anionic DNA and surrounding dipolar water, and ions. Time-resolved fluorescence Stokes shift (TRFSS) experiments revealed anomalously slow solvation dynamics in DNA much beyond 100 ps that follow either power-law or slow multiexponential decay over several nanoseconds. The origin of such dispersed dynamics remains difficult to understand. Here we compare results of TRFSS experiments to molecular dynamics (MD) simulations of well-known 4′,6-diamidino-2-phenylindole (DAPI)/Dickerson-Drew DNA complex over five decades of time from 100 fs to 10 ns to understand the origin of such dispersed dynamics. We show that the solvation time-correlation function (TCF) calculated from 200 ns simulation trajectory (total 800 ns) captures most features of slow dynamics as measured in TRFSS experiments. Decomposition of TCF into individual components unravels that slow dynamics originating from dynamically coupled DNA-water motion, although contribution from coupled water-Na + motion is non-negligible. The analysis of residence time of water molecules around the probe (DAPI) reveals broad distribution from ∼6 ps to ∼3.5 ns: Several (49 nos.) water molecules show residences time greater than 500 ps, of which at least 14 water molecules show residence times of more than 1 ns in the first solvation shell of DAPI. Most of these slow water molecules are found to occupy two hydration sites in the minor groove near DAPI binding site. The residence time of Na + , however, is found to vary within ∼17−120 ps. Remarkably, we find that freezing the DNA fluctuations in simulation eliminates slower dynamics beyond ∼100 ps, where water and Na + dynamics become faster, although strong anticorrelation exists between them. These results indicate that primary origin of slow dynamics lies within the slow fluctuations of DNA parts that couple with nearby slow water and ions to control the dispersed collective solvation dynamics in DNA minor groove.

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