The properties of advanced alumimium alloy systems

2XXX and 7XXX series aluminium alloys have been the accepted materials for airframe construction for many decades. However, only minor improvements in properties have been possible by the development of these alloys since the early 1970's. The constant need to reduce weight in aircraft has therefore led to a resurgence in the research for higher performance aluminium alloys. The reason for this investigation was to evaluate possible alternatives for the existing conventional aluminium alloy 2014 for aircraft wheel applications. Three new technologies in alloy development were considered: a metal matrix composite, an aluminium-lithium alloy and a powder metallurgical alloy. The basic mechanical properties of these advanced materials have already been established to an extent, but their fatigue behaviour has yet to be fully understood. The purpose of this work was to investigate the fatigue properties of the materials concerned, in both air and an aerated 3.5% NaCl solution, and compare these properties to 2014-T6. As well as the basic mechanical properties, fatigue crack propagation data is presented for all of the materials concerned. Additionally, fatigue crack initiation data is presented for the aluminium-lithium alloy and 2014. The D.C. electrical potential method was used to monitor crack growth. Of the materials investigated, the most promising was the aluminium-lithium alloy. However, short transverse properties need to be increased and the commercial cost of the material needs to be decreased before it can be considered as a direct replacement for 2014 for aircraft structural applications. It was considered that the cost of the powder metallurgical alloy would limit its further use. The metal matrix composite material proved to be unsuitable for most ambient temperature applications

Microstructural and environmental effects on fatigue crack propagation in duplex stainless steels

Fatigue crack initiation and propagation in duplex stainless steels are strongly affected by microstructure in both inert and aggressive environments. Fatigue crack growth rates in wrought Zeron 100 duplex stainless steel in air were found to vary with orientation depending on the frequency of crack tip retardation at ferrite/austenite grain boundaries. Fatigue crack propagation rates in 3.5% NaCl solution and high purity water are increased by hydrogen assisted transgranular cyclic cleavage of the ferrite. The corrosion fatigue results are interpreted using a model for the cyclic cleavage mechanism.

APP controls the formation of PI(3,5)P2 vesicles through its binding of the PIKfyve complex

Phosphoinositides are signalling lipids that are crucial for major signalling events as well as established regulators of membrane trafficking. Control of endosomal sorting and endosomal homeostasis requires phosphatidylinositol-3-phosphate (PI(3)P) and phosphatidylinositol-3,5-bisphosphate (PI(3,5)P2), the latter a lipid of low abundance but significant physiological relevance. PI(3,5)P2 is formed by phosphorylation of PI(3)P by the PIKfyve complex which is crucial for maintaining endosomal homeostasis. Interestingly, loss of PIKfyve function results in dramatic neurodegeneration. Despite the significance of PIKfyve, its regulation is still poorly understood. Here we show that the Amyloid Precursor Protein (APP), a central molecule in Alzheimer’s disease, associates with the PIKfyve complex (consisting of Vac14, PIKfyve and Fig4) and that the APP intracellular domain directly binds purified Vac14. We also show that the closely related APP paralogues, APLP1 and 2 associate with the PIKfyve complex. Whether APP family proteins can additionally form direct protein–protein interaction with PIKfyve or Fig4 remains to be explored. We show that APP binding to the PIKfyve complex drives formation of PI(3,5)P2 positive vesicles and that APP gene family members are required for supporting PIKfyve function. Interestingly, the PIKfyve complex is required for APP trafficking, suggesting a feedback loop in which APP, by binding to and stimulating PI(3,5)P2 vesicle formation may control its own trafficking. These data suggest that altered APP processing, as observed in Alzheimer’s disease, may disrupt PI(3,5)P2 metabolism, endosomal sorting and homeostasis with important implications for our understanding of the mechanism of neurodegeneration in Alzheimer’s disease.

The susceptibility of various UK aggregates to alkali silica reaction

A group of lithologically varied UK aggregates have been incorporated into concrete prisms of variable alkali content to ascertain the alkali levels at which significant ASR first occurs at 38oC and 100% RH. Petrographical analysis was used to establish the source of reactivity. The results of these expansion tests showed that significant ASR can develop with certain aggregates at initial alkali levels as low as 3.5 kg/m3 Na2Oe. Similar prisms were made at initial alkali levels, well above, on and just below the alkali thresholds for each aggregate. These prisms were placed in salt solution to establish the effects of ASR. The results showed that an external source of NaCl does accentuate ASR in high alkali mixes. However, in low alkali mixes the ASR initiated was even greater than that developed by the high alkali mixes. It was proposed that an `initial alkali pessimum' existed for each aggregate type for specimens placed in salt solution. Electron microprobe analysis of the ASR gels from concretes immersed in salt solution, showed that two compositionally varied gel suites develop. The first suite was derived from ASR caused by the initial alkalis in a concrete mix and was identical to ASR gels derived from the various concretes when immersed in distilled water. The second suite was developed by alkalis derived from a reaction between NaCl and the C3A component of the cement paste. It was demonstrated that the `initial alkali pessimum' was probably due to a combination of these two ASR types at the alkali threshold point where both suites of ASR gel can develop. Equivalent mixes were made with a 25% replacement of the cement by pulverised fuel ash (pfa) to establish whether alkalis released from the pfa could initiate ASR in otherwise non-reactive low alkali mixes. The addition of air entrainment to reactive concrete mixes was also examined as a method of suppressing ASR.

The mammalian phosphatidylinositol 3-phosphate 5-kinase (PIKfyve) regulates endosome-to-TGN retrograde transport

The yeast gene fab1 and its mammalian orthologue Pip5k3 encode the phosphatidylinositol 3-phosphate [PtdIns(3)P] 5-kinases Fab1p and PIKfyve, respectively, enzymes that generates phosphatidylinositol 3,5-bisphosphate [PtdIns(3,5)P(2)]. A shared feature of fab1Delta yeast cells and mammalian cells overexpressing a kinase-dead PIKfyve mutant is the formation of a swollen vacuolar phenotype: a phenotype that is suggestive of a conserved function for these enzymes and their product, PtdIns(3,5)P(2), in the regulation of endomembrane homeostasis. In the current study, fixed and live cell imaging has established that, when overexpressed at low levels in HeLa cells, PIKfyve is predominantly associated with dynamic tubular and vesicular elements of the early endosomal compartment. Moreover, through the use of small interfering RNA, it has been shown that suppression of PIKfyve induces the formation of swollen endosomal structures that maintain their early and late endosomal identity. Although internalisation, recycling and degradative sorting of receptors for epidermal growth factor and transferrin was unperturbed in PIKfyve suppressed cells, a clear defect in endosome to trans-Golgi-network (TGN) retrograde traffic was observed. These data argue that PIKfyve is predominantly associated with the early endosome, from where it regulates retrograde membrane trafficking to the TGN. It follows that the swollen endosomal phenotype observed in PIKfyve-suppressed cells results primarily from a reduction in retrograde membrane fission rather than a defect in multivesicular body biogenesis.