Power demand and energy usage of container crane - comparison between AC and DC drives

The electrical data of two quay cranes, one has a DC drive system and the other has an AC drive system, in actual working conditions at a container terminal are measured and presented in this paper. Peak demand, energy usage, power factor and power quality are examined and compared.

A new H.E.L.P kit for teaching practical AC electronics to undergraduate distance students

An important part of educating students in electronics and electrical engineering is laboratory practicals. Providing effective practical experience to students by distance education has always been a significant challenge to the engineering educator. Deakin University has for many years taught practicals in basic digital electronics to off-campus students by means of a kit. The same students have performed related exercises in analogue electronics, which require generating and measuring AC signals, by means of either software simulations or on-campus attendance at lab classes. This year, for the first time, off-campus students are being provided with a new kit, which contains a low-cost, battery-powered AC signal generator, and an interface that allows a PC to be used as an oscilloscope. This kit allows the off-campus student further flexibility in learning basic electronics.

Multiple vesicular morphologies in AB/AC diblock copolymer complexes through hydrogen bonding interactions

We report for the first time multiple vesicular morphologies in block copolymer complexes formed in aqueous media via hydrogen bonding interactions. A model AB/AC diblock copolymer system consisting of polystyrene-block- poly(acrylic acid) (PS-b-PAA) and polystyrene-block-poly(ethylene oxide) (PS-b-PEO) was examined using transmission electron microscopy, small-angle X-ray scattering, and dynamic light scattering. The complexation and morphological transitions were driven by the hydrogen bonding between the complementary binding sites on PAA and PEO blocks of the two diblock copolymers. Upon the addition of PS-b-PEO, a variety of bilayer aggregates were formed in PS-b-PAA/PS-b-PEO complexes including vesicles, multilamellar vesicles (MLVs), thick-walled vesicles (TWVs), interconnected compound vesicles (ICCVs), and irregular aggregates. Among these aggregates, ICCVs were observed as a new morphology. The morphology of aggregates was correlated with respect to the molar ratio of PEO to PAA. At [EO]/[AA] = 0.5, vesicles were observed, while MLVs were obtained at [EO]/[AA] = 1. TWVs and ICCVs were formed at [EO]/[AA] = 2 and 6, respectively. When [EO]/[AA] reached 8 and above, only irregular aggregates appeared. These findings suggest that complexation between two amphiphilic diblock copolymers is a viable approach to prepare polymer vesicles in aqueous media.

Reperfusion-induced myocardial dysfunction is prevented by endogenous annexin-A1 and its N-terminal-derived peptide Ac-ANX-A12-26

BACKGROUND AND PURPOSE : Annexin-A1 (ANX-A1) is an endogenous, glucocorticoid-regulated anti-inflammatory protein. The N-terminal-derived peptide Ac-ANX-A12–26 preserves cardiomyocyte viability, but the impact of ANX-A1-peptides on cardiac contractility is unknown. We now test the hypothesis that ANX-A1 preserves post-ischaemic recovery of left ventricular (LV) function.

EXPERIMENTAL APPROACH : Ac-ANX-A12–26 was administered on reperfusion, to adult rat cardiomyocytes as well as hearts isolated from rats, wild-type mice and mice deficient in endogenous ANX-A1 (ANX-A1–/–). Myocardial viability and recovery of LV function were determined.

KEY RESULTS: Ischaemia–reperfusion markedly impaired both cardiomyocyte viability and recovery of LV function by 60%. Treatment with exogenous Ac-ANX-A12–26 at the onset of reperfusion prevented cardiomyocyte injury and significantly improved recovery of LV function, in both intact rat and wild-type mouse hearts. Ac-ANX-A12–26 cardioprotection was abolished by either formyl peptide receptor (FPR)-nonselective or FPR1-selective antagonists, Boc2 and cyclosporin H, but was relatively insensitive to the FPR2-selective antagonist QuinC7. ANX-A1-induced cardioprotection was associated with increased phosphorylation of the cell survival kinase Akt. ANX-A1−/− exaggerated impairment of post-ischaemic recovery of LV function, in addition to selective LV FPR1 down-regulation.

CONCLUSIONS AND IMPLICATIONS : These data represent the first evidence that ANX-A1 affects myocardial function. Our findings suggest ANX-A1 is an endogenous regulator of post-ischaemic recovery of LV function. Furthermore, the ANX-A1-derived peptide Ac-ANX-A12–26 on reperfusion rescues LV function, probably via activation of FPR1. ANX-A1-based therapies may thus represent a novel clinical approach for the prevention and treatment of myocardial reperfusion injury.