Polymorphonuclear leukocytes (PMN) degranulate, adhere to vascular endothelium, or aggregate to each other following exposure of the cells to high concentrations of chemotactic stimuli such as formyl-methionyl- leucyl phenylalanine (FMLP). PMN released the specific granule product lactoferrin more readily in response to chemotactic stimuli, which correlated with promotion of PMN aggregation as measured by light transmission and enhanced PMN adherence. Both concanavalin A (Con-A) and phorbol myristate acetate (PMA), agents that lead to specific granule discharge, induced and sustained human PMN aggregation. Similarly, supernatants, generated from Con-A-treated PMN, aggregated fresh PMN in the presence of alpha-methylmannoside, a competitive inhibitor of the lectin. Anti-human lactoferrin IgG but not normal goat IgG blunted the aggregation elicited by both PMA and FMLP. Both human milk lactoferrin and rabbit PMN lactoferrin aggregated human lactoferrin promoted PMN adherence to endothelial cells. The enhanced PMN stickiness was correlated with the early phase of degranulation. Thus, PMN lactoferrin serves an autoregulatory role to retain PMN at inflammatory sites to amplify the inflammatory response.
A B S T R A C T The present study aims at explaining the synergistic effect of environmental media and stress/strain on fatigue lives of aluminium alloys. Rotating bending fatigue tests were carried out using four different aluminium alloys LY12-CZ, 2024-T4, 7475-T7351 and 7075-T651, at air state, 3.5% and 5.0% NaCl aqueous solutions. These results indicated that synergistic actions of the environmental media and cyclic loading accelerated the fatigue crack propagation of aluminium alloys. Furthermore, various influence factors (such as solution concentration, cyclic numbers, high (low) strength aluminium alloys etc.) of the fatigue life at synergistic actions of the environmental media and stress were quantificationally discussed in this paper.Keywords aluminium alloy; corrosion environment; fatigue life; fracture behaviour; synergistic effect. N O M E N C L A T U R Eα = the stress concentration factor (1.08) B, C = the distance between adjacent striations, respectively d, L = the geometry size, respectively g = the acceleration of gravity (9.8 m/s 2 ) N f = number of cycles to failure σ = stress amplitude (MPa) R = stress ratio I N T R O D U C T I O NThere have been growing interests in light metals, such as aluminium, magnesium and titanium-aluminium alloys, which have been widely applied to aeronautic and automotive industries because of their high strength-toweight ratios, 1-3 but improvements are needed in their fatigue properties, 4-8 very high-cycle fatigue behaviour of aluminium alloys 9-11 and some factors of high humidity on fatigue properties of aluminium alloys. 12As one of the important materials in aeronautic and automotive structures, the aluminium alloy is usually directly exposed to the corrosive environment with stress/strain, 13 in which the corrosive fatigue cracking mechanism is rather a complex process and needs to be deeply understood. More data, especially fatigue properties in such an environment, are crucial for safety. In recent years, many studies have focused on the fatigue behaviour of Al alloys in the corrosive environment.14 Li et al. 15estimated the effect of pre-corrosion states on the fatigue microcrack initiation and early stage propagation behaviour of 6151-T6 aluminium alloy based on scanning electron microscopy (SEM) in situ observation. Hui et al. 16 and Qian et al.14 conducted fatigue life tests in the laboratory air and salt water environment by using several pre-corrosion 7XXX aluminium alloys and a structural steel 40Cr and reported that the salt water environment significantly reduced the fatigue performance, especially under low stress amplitude and the fatigue life is about 2.2% of that at air state. These results indicated that the effect of different pre-corrosion states on the fatigue damage of aluminium alloys is mainly producing more stress concentration sites (or pits) and inducing more fatigue cracks. Zhang et al. 17proposed a novel model to predict the residual fatigue life of 2A12 aluminium alloy subjected to alternating corrosion and fatigue based on the ...
Aim To measure the stress levels of Doctor of Veterinary Medicine (DVM) students at the University of Sydney using the Kessler Psychological Distress Scale (K10) questionnaire.Methods DVM students in years 1 to 4 were surveyed in semester 2 of 2018. The voluntary online survey consisted of 6 demographic questions and the K10 scale, a standardised measure of stress commonly used in Australia by medical practitioners for evaluation and referral to mental health professionals. Academic year cohorts were compared to identify differences in stress levels. Cohorts were compared to published K10 scores from various populations including the Australian public, medical students, practicing veterinarians, and Junior Medical Officers (JMOs). ResultsThe response rate was 54.4% (n = 237). DVM students experienced a higher level of psychological distress (mean 24, median 23, range 10-50) than the Australian population (mean 14.5, median 13, range 10-50), medical students (mean 18.4, median 16, range 10-50), practicing veterinarians (mean 16.7, median 15.5, range 10-30), and JMOs (mean 18.1, median 16, range 10-50). Female students (median 23) had a significantly higher level of psychological distress compared to male students (median 18) (p = 0.0005). International students (median 23) had a higher level of psychological stress than domestic students (median 22) (p = 0.0488). Different year cohorts, age range, work hours, and exercise were not associated with difference in stress levels.Conclusion Based on higher levels of stress in DVM students than that of the general population, practicing veterinarians, JMOs and medical students, there is an urgent need for evidencebased interventions to target stress in DVM students.
The reaction of FMLP with granulocytes causes aggregation and degranulation and enhances adherence to endothelium. To evaluate whether prevention of granule extrusion could impair these granulocyte activities, granulocytes were treated with either dexamethasone or hydrocortisone prior to treatment with FMLP. Dexamethasone was added to suspensions of cytochalasin B-treated granulocytes; it markedly impaired the aggregation response of the granulocytes of FMLP. When cytochalasin-B was not used, granulocyte aggregation in response to FMLP or PMA was inhibited by dexamethasone. Although dexamethasone prevented aggregation of cells following stimulation with FMLP or PMA, it failed to prevent the aggregation of granulocytes induced by rabbit lactoferrin. Adherence of granulocytes to human endothelial monolayers was enhanced by FMLP; dexamethasone inhibited the enhancement. However, with the addition of human lactoferrin to the granulocytes exposed to dexamethasone, the cells were able to adhere as well to endothelium as the cells exposed to FMLP but free of dexamethasone. When cytochalasin- B-treated granulocytes were incubated with dexamethasone or hydrocortisone prior to the addition of FMLP, the subsequent release of lactoferrin was substantially blocked, whereas the release of the primary granule products, lysozyme and beta-glucuronidase, was attenuated but not completely blocked. Thus, corticosteroids might block chemotactic-factor-induced granulocyte aggregation by selectively preventing release of specific granule products that contribute to and sustain aggregation.
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