a b s t r a c tFor high-strength steels, the crack initiation of very-high-cycle fatigue (VHCF) is commonly at the interior of material with fish-eye (FiE) morphology containing a fine-granular-area (FGA) surrounding an inclusion as crack origin, and FGA is regarded as the characteristic region of crack initiation. Here, we carefully examined the micro-morphology of FGA and FiE for two high-strength steels. The results revealed that the microscopic nature of FGA is a thin layer of nanograins. Then we proposed the formation mechanism of FGA: Numerous Cyclic Pressing (NCP) between originated crack surfaces, which causes grain refinement at originated crack wake and therefore the formation of FGA. The results of second set experiment showed that the cases with negative stress ratios exhibit the prevalence of nanograin layer in FGA region and the nanograin layer vanishes for the cases with positive stress ratios, which is a verification of the proposed NCP model.

Fatigue tests of a high carbon chromium steel were performed using rotating bending and ultrasonic axial cycling. Fatigue crack initiated at specimen interior for very-high-cycle fatigue (VHCF) with fish-eye pattern embracing fine-granular-area (FGA) originated from inclusion. The fatigue life from FGA to fish-eye and from fish-eye to the critical crack size was respectively calculated, so as to estimate the fatigue life contributed by FGA. The crack extension rate within FGA was also estimated. Our results demonstrated that the formation of FGA is responsible for a majority part of total fatigue life.

Defensive responses to threatening stimuli are crucial to the survival of species. While expression of these responses is considered to be instinctive and unconditional, their magnitude may be affected by environmental and internal factors. The neural circuits underlying this modulation are still largely unknown. In mice, looming-evoked defensive responses are mediated by the superior colliculus (SC), a subcortical sensorimotor integration center. We found that repeated stress caused an anxiety-like state in mice and accelerated defensive responses to looming. Stress also induced c-fos activation in locus coeruleus (LC) tyrosine hydroxylase (TH) neurons and modified adrenergic receptor expression in SC, suggesting a possible Th::LC-SC projection that may be involved in the accelerated defensive responses. Indeed, both anterograde and retrograde neural tracing confirmed the anatomical Th::LC-SC projection and that the SC-projecting TH neurons in LC were activated by repeated stress. Optogenetic stimulation of either LC TH neurons or the Th::LC-SC fibers also caused anxiety-like behaviors and accelerated defensive responses to looming. Meanwhile, chemogenetic inhibition of LC TH neurons and the infusion of an adrenergic receptor antagonist in SC abolished the enhanced looming defensive responses after repeated stress, confirming the necessity of this pathway. These findings suggest that the Th::LC-SC pathway plays a key role in the sophisticated adjustments of defensive behaviors induced by changes in physiological states.