Effect of susceptibility to interfacial fracture on fatigue properties of spot-welded high strength sheet steel

While advanced high strength steels (AHSS) have numerous advantages for the automotive industry, they can be susceptible to interfacial fracture when spot-welded. In this study, the susceptibility of interfacial fracture to spot-weld microstructure and hardness is examined, as well as the corresponding relationships between fatigue, overload performance, and interfacial fracture for a TRIP (transformation induced plasticity) steel. Simple post-weld heat-treatments were used to alter the weld microstructure. The effect on interfacial fracture of diluting the weld pool by welding the TRIP material to non-TRIP steel was examined, along with the effect of altering the base material microstructure. Results show that weld hardness is not a good indicator of either the susceptibility to interfacial fracture, or the strength of the joint, and that interfacial fracture does not necessarily lead to a decrease in strength compared to conventional weld-failure mechanisms, i.e. button pullout. It was also found that while interfacial fracture does affect low cycle to failure behavior, there was no effect on high cycle fatigue.

Does cigarette promotion increase susceptibility to smoking? : a re-test of the link between tobacco industry promotion and adolescent susceptibility to cigarette use

In 1998, using the Index of Receptivity to Tobacco Industry Promotion (IRTIP), it was claimed that tobacco promotion increased youth susceptibility to smoking. Arguably, this claim started the belief that ?cigarette advertising causes smoking? and led to many countries severely restricting cigarette promotion. The problem is, ten years lat... more »er, youth are still lighting up. Could they have gotten it wrong? The IRTIP procedure is widely used to model the link between promotional activities and susceptibility to product use. It is now being used for other products like alcohol, fast-food and colas. This book reports the results of a verification and re-test of the IRTIP model. Using the original data, it was found that IRTIP magnifies Response-Style and Respondent Drop-Out Biases. These biases are shown to lead to the finding of a positive link between tobacco promotion and susceptibility to smoking. Because the IRTIP process is biased, it may be prudent to revisit the many research studies that have used this procedure. The faulty 1998 claim may have harmed efforts to control and limit the use of cigarettes.

Re-testing the link between youth receptivity to tobacco promotion and their susceptibility to smoke

The Index of Receptivity to Tobacco Industry Promotion (IRTIP) is a model that is used by hundreds of articles. The causal claim based on findings from this model is even more pervasive, and has resulted in much of the modern post 1998 tobacco legislation that is still enforced. This thesis tested the link between adolescent receptivity to tobacco industry promotion and susceptibility to smoking. Pierce et al. (1998) reported that they had found a positive and causal association between receptivity and susceptibility by using IRTIP. They claimed that receptivity to tobacco industry promotion was the only significant causal factor affecting adolescent susceptibility to smoking. Exposure to peer and parental smoking was not found to be a significant effect. A review of the literature found that many sections of IRTIP differ from accepted marketing theory on how cigarette advertising and promotions affect adolescent adoption of cigarette smoking. The proxy measures used in IRTIP were shown to diverge from those previously used for measuring the constructs of Attention, Intention, Desire and Action (AIDA) in marketing communications. IRTIP also differs from previous theory by including measures that attempt to quantify the effect of tobacco premiums into a model that was designed to measure the effects of advertising.

Extreme response bias in measuring susceptibility to smoking.

Pierce, Choi, Gilpin, Farkas, and Berry (1998) were the first to claim that they could provide causal evidence that tobacco industry advertising and promotion caused adolescent smoking. This claim continues to significantly influence the theory and conceptualization of how youth react to tobacco marketing. The Pierce et al. (1998) methodology has been used by many researchers to establish the influence of tobacco marketing on adolescent smoking (Goldberg, 2003; NCI, 2006; Sargent, Dalton, & Beach, 2000). Pierce et al. (1998) selected respondents for only the second of their two survey longitudinal study because they chose the extreme-negative response. This choice could be the result of the tendency of some significant number of sample members exhibiting extreme-response bias. The results from an analysis of several questions from the original data used by Pierce et al. (1998) has suggested that there is a significant extreme-response style pattern in the Pierce et al. data. This unaccounted for bias in the responses of their sample was due to the procedure used by Pierce et al. (1998) in the selection of their respondents. The Pierce et al. (1998) sample selection procedure requires more research before the causal link can be claimed.

Individual differences predict susceptibility to conditioned fear arising from psychosocial trauma

Background : Classical Pavlovian fear conditioning has been widely used in preclinical studies to gain insights into anxiety-related disorders. In this study we examined whether pre-existing behavioral differences, and/or behavioral differences displayed during fear induction, predict the severity of the conditioned fear response that can develop after an episode of psychosocial conflict.

Methods : Prior to conditioning, male rats (intruders) were behaviorally assessed using the novel environment exploration and defensive burying tests. These animals were subsequently placed in the territory of an older male (resident) that invariably attacked the intruder.

Results : Upon return to this territory 24 h later, intruders moved less than controls and produced more distress vocalizations, indicating conditioned fear to context. Additionally, analyses revealed that both pre-existing behavioral differences, and the animal’s response during social conflict, predicted the magnitude of the subsequent conditioned fear response. Specifically, animals that engaged in higher levels of novel environment exploration, that exhibited a greater number of defensive burying behaviors, and that demonstrated higher levels of fighting and guarding during social conflict, displayed less evidence of conditioned fear.

Conclusion : These findings show that the behavioral variability existent within a normal outbred population can predict the magnitude of the conditioned fear response.

Strain differences in coping behaviour, novelty seeking behaviour, and susceptibility to socially conditioned fear : a comparison between Wistar and Sprague Dawley rats

The aim of the current study was to generate socially conditioned fear in two different strains of rat (Wistar, W and Sprague Dawley, SD) using social conflict, in order to investigate whether the magnitude of the conditioned fear responses in each strain was related to behaviour exhibited prior to or during fear induction (i.e. social conflict). On day one of the study, all intruders were assessed for exploratory activity in a novel environment. Twenty four hours following the novel environment test the locomotor activity of the intruders was assessed, while they underwent a single familiarisation exposure to the arena in which the conflict was subsequently to occur in. Twenty-four hours following familiarisation, intruders underwent either a 10 min social conflict or sham conflict session. One day later we examined the response of the intruders when they were returned to the vacant resident's cage. Upon return to the conflict context, we examined the intruder's ultrasonic distress vocalisations and the extent to which locomotor activity was inhibited. We found that W rats displayed significantly more immobility (i.e. conditioned fear) upon return to context than did SD rats (p < 0.05). Importantly, we observed that the differences in the two strains behaviour upon return to context appeared to be related to their quite different patterns of coping behaviour. The results of the current study indicate that preclinical between-strain comparisons potentially have much to offer in regard to understanding the basis of resilience to social stress.

High glucose-induced impairment in insulin secretion is associated with reduction in islet glucokinase in a mouse model of susceptibility to islet dysfunction

Type 2 diabetes is characterized by islet dysfunction resulting in hyperglycemia, which can then lead to further deterioration in islet function. A possible mechanism for hyperglycemia-induced islet dysfunction is the accumulation of advanced glycation end products (AGE). The DBA/2 mouse develops pancreatic islet dysfunction when exposed to a high glucose environment and/or obesity-induced insulin resistance. To determine the biochemical cause of dysfunction, DBA/2 and C57BL/6 control islets were incubated in 11.1 mM or 40 mM glucose in the absence or presence of the AGE inhibitor aminoguanidine (AG) for 10 days. Basal (2.8 mM glucose) insulin release was increased in both DBA/2 and C57BL/6 islets incubated with 40 mM vs 11.1 mM glucose for 10 days. Chronic exposure to hyperglycemia decreased glucose (20 mM)-stimulated insulin secretion in DBA/2 but not in C57BL/6 islets. AG significantly increased fold-induced insulin release in high glucose cultured DBA/2 mouse islets, but did not affect C57BL/6 islet function. DBA/2 islet glucokinase was significantly reduced following 40 mM glucose culture, compared with 11.1 mM glucose cultured DBA/2 islets and 40 mM glucose cultured C57BL/6 islets. Incubation of islets with AG resulted in a normalization of DBA/2 islet glucokinase levels. In conclusion, chronic high glucose-induced increases in AGE can result in islet dysfunction and this is associated with reduced glucokinase levels in a mouse model with susceptibility to islet failure.

Blood pressure modifies retinal susceptibility to intraocular pressure elevation

Primary open angle glaucoma affects more than 67 million people. Elevated intraocular pressure (IOP) is a risk factor for glaucoma and may reduce nutrient availability by decreasing ocular perfusion pressure (OPP). An interaction between arterial blood pressure and IOP determines OPP; but the exact contribution that these factors have for retinal function is not fully understood. Here we sought to determine how acute modifications of arterial pressure will affect the susceptibility of neuronal function and blood flow to IOP challenge. Anaesthetized (ketamine:xylazine) Long-Evan rats with low (~60 mmHg, sodium nitroprusside infusion), moderate (~100 mmHg, saline), or high levels (~160 mmHg, angiotensin II) of mean arterial pressure (MAP, n = 5–10 per group) were subjected to IOP challenge (10–120 mmHg, 5 mmHg steps every 3 minutes). Electroretinograms were measured at each IOP step to assess bipolar cell (b-wave) and inner retinal function (scotopic threshold response or STR). Ocular blood flow was measured using laser-Doppler flowmetry in groups with similar MAP level and the same IOP challenge protocol. Both b-wave and STR amplitudes decreased with IOP elevation. Retinal function was less susceptible to IOP challenge when MAP was high, whereas the converse was true for low MAP. Consistent with the effects on retinal function, higher IOP was needed to attenuated ocular blood flow in animals with higher MAP. The susceptibility of retinal function to IOP challenge can be ameliorated by acute high BP, and exacerbated by low BP. This is partially mediated by modifications in ocular blood flow.