Effects of fatigue-induced changes in microstructure and stress on domain structure and magnetic properties of Fe–C alloys

A study of the effects of microstructural changes on domain structure and magnetic properties as a result of fatigue has been made on Fe–C alloys subjected to either cold work, stress-relief annealing, or heat treatment that produced a ferritic/pearlitic structure. The magnetic properties varied with stress cycling depending on the initial condition of the samples. Variations in coercivity in the initial stage of fatigue were closely related to the changes in dislocation structure. In the intermediate stage of fatigue the observed refinement of domain structures was related to the development of dislocation cell structures and formation of slip bands. In the final stage of fatigue the remanence and maximum permeability decreased dramatically, and this rate of decrease was dependent on the crack propagation rate

SAFOD Phase III Core Sampling and Data Management at the Gulf Coast Repository

The San Andreas Fault Observatory at Depth (SAFOD)project is yielding new insight into the San Andreas Fault (Zoback et al., 2010; Zoback et al., this issue). SAFOD drilling started in 2002 with a pilot hole, and proceeded with three phrases of drilling and coring during the summers of 2004, 2005, and 2007 (Fig. 1). One key component of theproject is curation, sampling, and documentation of SAFOD core usage at the Integrated Ocean Drilling Program’s (IODP) Gulf Coast Repository (GCR) at Texas A&M University. We present here the milestones accomplished over the past two years of sampling Phase III core at the GCR

Monitoring fatigue damage in materials using magnetic measurement techniques

Measurements of hysteresis and Barkhausen effect (BE) have been made on 0.1 wt % C Fe–C alloys subjected to strain-controlled fatigue at various strain amplitudes. A relationship between the fatigue lifetime and strain amplitude was observed. The hysteresis properties of the samples cycled at different strain amplitudes were found to vary systematically with expended fatigue life. These properties showed significant changes in the initial and final stages of fatigue, while between these stages they remained stabilized. In the stable stage the remanence was found to decrease, whereas the coercivity increased with increasing strain amplitude. Variations in BE signal during fatigue were found to be closely related to the microstructural changes observed on the sample surface. These results are interpreted in the context of the changes in microstructure caused by fatigue damage, and the effects of the formation and propagation of fatigue cracks on the field distribution and domain structure in the vicinity of the cracks

Social Rejection Magnifies Impulsive Behavior Among Individuals with Greater Negative Urgency: An Experimental Test of Urgency Theory

Impulsivity is a multifaceted trait with substantial implications for human well-being. One facet of impulsivity is negative urgency, the tendency to act impulsively in response to negative affect. Correlational evidence suggests that negative affect magnifies impulsive behavior among individuals with greater negative urgency, yet causal evidence for this core pillar of urgency theory is lacking. To fill this gap in the literature, participants (N = 363) were randomly assigned to experience social rejection (a situation shown to induce negative affect) or acceptance. Participants then reported their subjective negative affect, completed a behavioral measure of impulsivity, and reported their negative urgency. Among individuals with relatively high and average negative urgency, social rejection increased their impulsive behavior through greater experiences of negative affect. These indirect effects were not observed among individuals relatively low in negative urgency. These findings suggest that negative urgency exists at the nexus of urgent dispositions and situations that elicit negative affect, which offers novel support for urgency theory

Physical Aggressiveness and Gray Matter Deficits in Ventromedial Prefrontal Cortex

What causes individuals to hurt others? Since the famous case of Phineas Gage, lesions of the ventromedial prefrontal cortex (VMPFC) have been reliably linked to physically aggressive behavior. However, it is unclear whether naturally-occurring deficits in VMPFC, among normal individuals, might have widespread consequences for aggression. Using voxel based morphometry, we regressed gray matter density from the brains of 138 normal female and male adults onto their dispositional levels of physical aggression, verbal aggression, and sex, simultaneously. Physical, but not verbal, aggression was associated with reduced gray matter volume in the VMPFC and to a lesser extent, frontopolar cortex. Participants with less gray matter density in this VMPFC cluster were much more likely to engage in real-world violence. These findings suggest that even granular deficits in normal individuals’ VMPFC gray matter can promote physical aggression

The Optimal Calibration Hypothesis: How Life History Modulates the Brain\u27s Social Pain Network

A growing body of work demonstrates that the brain responds similarly to physical and social injury. Both experiences are associated with activity in the dorsal anterior cingulate cortex (dACC) and anterior insula. This dual functionality of the dACC and anterior insula underscores the evolutionary importance of maintaining interpersonal bonds. Despite the weight that evolution has placed on social injury, the pain response to social rejection varies substantially across individuals. For example, work from our lab demonstrated that the brain\u27s social pain response is moderated by attachment style: anxious-attachment was associated with greater intensity and avoidant-attachment was associated with less intensity in dACC and insula activation. In an attempt to explain these divergent responses in the social pain network, we propose the optimal calibration hypothesis, which posits variation in social rejection in early life history stages shifts the threshold of an individual\u27s social pain network such that the resulting pain sensitivity will be increased by volatile social rejection and reduced by chronic social rejection. Furthermore, the social pain response may be exacerbated when individuals are rejected by others of particular importance to a given life history stage (e.g., potential mates during young adulthood, parents during infancy and childhood)

Neural Mechanisms of the Rejection-Aggression Link

Social rejection is a painful event that often increases aggression. However, the neural mechanisms of this rejection–aggression link remain unclear. A potential clue may be that rejected people often recruit the ventrolateral prefrontal cortex’s (VLPFC) self-regulatory processes to manage the pain of rejection. Using functional MRI, we replicated previous links between rejection and activity in the brain’s mentalizing network, social pain network and VLPFC. VLPFC recruitment during rejection was associated with greater activity in the brain’s reward network (i.e. the ventral striatum) when individuals were given an opportunity to retaliate. This retaliation-related striatal response was associated with greater levels of retaliatory aggression. Dispositionally aggressive individuals exhibited less functional connectivity between the ventral striatum and the right VLPFC during aggression. This connectivity exerted a suppressing effect on dispositionally aggressive individuals’ greater aggressive responses to rejection. These results help explain how the pain of rejection and reward of revenge motivate rejected people to behave aggressively