Study of effect on tensile stress test from distortion of fibre laser welded Ti6Al4V using FEA

Distortion is one type of defect in the weld, which is troublesome for some reasons, especially in thin plate welding. Distortion was found in fibre laser welding processing for 0.7mm thickness Ti6Al4V plate. The purpose of this paper is to understand and evaluate the effect of distortion on stress level by FEA and tensile test. A group of 0.7mm Ti6Al4V plates welded using continuous wave fibre laser. FEA models were established for fibre laser welded Ti6Al4V in abaqus 6.7. © (2011) Trans Tech Publications.

Acoustic emission and yield in sand

An experimental investigation into the Acoustic Emission (AE) response of sand has been undertaken, and the use of AE as a method of yield point identification has been assessed. Dense, saturated samples of sand were tested in conventional triaxial apparatus. The measurements of stresses and strains were carried out according to current research practice. The AE monitoring system was integrated with the soil mechanics equipment in such a way that sample disturbance was minimised. During monotonically loaded, constant cell pressure tests the total number of events recorded was found to increase at an increasing rate in a manner which may be approximated by a power law. The AE response of the sand was found to be both stress level and stress path dependent. Undrained constant cell pressure tests showed that, unlike drained tests, the AE event rate increased at an increasing rate; this was shown to correlate with the mean effective stress variation. The stress path dependence was most noticeable in extension tests, where the number of events recorded was an order of magnitude less than that recorded in comparable compression tests. This stress path dependence was shown to be due to the differences in the work done by the external stresses. In constant cell pressure tests containing unload/reload cycles it was found that yield could be identified from a discontinuity in the event rate/time curve which occurred during reloading. Further tests involving complex stress paths showed that AE was a useful method of yield point identification. Some tests involving large stress reversals were carried out, and AE identified the inverse yield points more distinctly than conventional methods of yield point identification.

The mechanics of creep crack growth in a Magnox alloy

Magnox AL80 has been used for a study of creep crack propagation. A number of variables have been considered such as specimen geometry,notch root radius, material thickness, creep prestrain and stress level.The work has covered the material behaving under two values of the creep exponent, n=3.5 and n=7, according to the stress level. As well as observing initiation times and crack growth rates, scribed grids have been used to examine the near crack tip strain levels and distributions. It was shown that estimations of COD from notch flank opening can give misleading indications of material behaviour and that a more informative method was to monitor displacements in the material surrounding the crack tip. Strong evidence was found for crack advance being displacement controlled, however it was shown that the COD approach should be considered geometry dependant. The summation of ∈xx and ∈yy provided the most successful description of crack advance as it produced a single value that described propagation in all the cases concidered. The strain distributions indicates that σyy was related to distance from a point ahead of the crack tip by the exponent - (l/n+l) and that σxx is proportional to σyy. The constraint stresses arising in the DEN and CN specimens were evaluated. Initiation time was found to be principally affected by the stress level but was modified by the constraints arising from specimen geometry. Crack growth was found not to obey either the empirical K or σpett relationships but was reviewed in context of the observed strain behaviour.

Fatigue crack propagation mechanisms in a thermally aged duplex stainless steel

Zeron 100 duplex stainless steel is susceptible to embrittlement following ageing at temperatures between 350 °C and 450 °C. The embrittlement is associated with cleavage of the age-hardened ferrite phase, initiated by deformation twinning. This can result in order of magnitude increases in the fatigue crack propagation rate. The effects of ageing on the mechanisms of fatigue crack propagation in Zero 100 are investigated, and a quantitative model is developed, accounting for the effects of hardness, temperature, stress level and microstructure on the fatigue crack growth rate. © 1994.

Development of a quality control material for the measurement of 8-oxo-7,8-dihydro-2'-deoxyguanosine, an in vivo marker of oxidative stress, and comparison of results from different laboratories

The measurement of 8-oxo-7,8-dihydro-2'-deoxyguanosine is an increasingly popular marker of in vivo oxidative damage to DNA. A random-sequence 21-mer oligonucleotide 5'-TCA GXC GTA CGT GAT CTC AGT-3' in which X was 8-oxo-guanine (8-oxo-G) was purified and accurate determination of the oxidised base was confirmed by a 32P-end labelling strategy. The lyophilised material was analysed for its absolute content of 8-oxo-dG by several major laboratories in Europe and one in Japan. Most laboratories using HPLC-ECD underestimated, while GC-MS-SIM overestimated the level of the lesion. HPLC-ECD measured the target value with greatest accuracy. The results also suggest that none of the procedures can accurately quantitate levels of 1 in 10(6) 8-oxo-(d)G in DNA.

Autonomic dysfunction and systemic oxidative stress associated with glaucomatous optic neuropathy

There were four principal sections to the work: 1. Investigation of ocular and systemic vascular risk factors in POAG. The principal findings of this work were: a). Glaucoma patients exhibit an anticipatory reaction to the physical stress, similar to subjects at risk for cardiovascular diseases; a blunted BP response and a reduction in ONH blood flow in response to cold provocation was also recorded. b). Silent myocardial ischaemic episodes occurred during peaks in systemic BP and HR. c). Independent of a positive history for cardiovascular diseases, patients suffering from POAG demonstrate a blunt circadian rhythm of the ANS. 2. Assessment of the relationship between vascular and systemic vascular risk factors in GON. The principal findings of this work were: a). POAG patients demonstrate a high sympathetic tonus over a 24-h period. b). POAG patients with lower OBF demonstrate both 24-h systemic BP and HRV abnormalities. c). OBF alterations observed in some glaucoma patients could be either primary or secondary to systemic haemodynamic disturbances and not a consequence of ONH damage. 3. Assessment of the level of systemic anti-oxidant defence in POAG patients. The principal finding of this work was: Patients suffering from POAG demonstrated significantly lower GSH and t-GSH levels than normal controls. 4. Investigation of the effect of treatment with latanoprost 0.005% on visual function and OBF. The findings of this work were: a). Treatment with latanoprost 0.005% resulted in a significant decrease in IOP and increase in OPP. VF damage progression has also been stopped. b). Treatment with latanoprost 0.005% resulted in a significant increase in the OBF parameters measured at the ONH and peripapillary retina levels. Finally, the importance of a clear protocol for managing new POAG cases is highlighted and a clinical conduit is proposed.

Gene network and proteomic analyses of cardiac responses to pathological and physiological stress

Background—The molecular mechanisms underlying similarities and differences between physiological and pathological left ventricular hypertrophy (LVH) are of intense interest. Most previous work involved targeted analysis of individual signaling pathways or screening of transcriptomic profiles. We developed a network biology approach using genomic and proteomic data to study the molecular patterns that distinguish pathological and physiological LVH. Methods and Results—A network-based analysis using graph theory methods was undertaken on 127 genome-wide expression arrays of in vivo murine LVH. This revealed phenotype-specific pathological and physiological gene coexpression networks. Despite >1650 common genes in the 2 networks, network structure is significantly different. This is largely because of rewiring of genes that are differentially coexpressed in the 2 networks; this novel concept of differential wiring was further validated experimentally. Functional analysis of the rewired network revealed several distinct cellular pathways and gene sets. Deeper exploration was undertaken by targeted proteomic analysis of mitochondrial, myofilament, and extracellular subproteomes in pathological LVH. A notable finding was that mRNA–protein correlation was greater at the cellular pathway level than for individual loci. Conclusions—This first combined gene network and proteomic analysis of LVH reveals novel insights into the integrated pathomechanisms that distinguish pathological versus physiological phenotypes. In particular, we identify differential gene wiring as a major distinguishing feature of these phenotypes. This approach provides a platform for the investigation of potentially novel pathways in LVH and offers a freely accessible protocol (http://sites.google.com/site/cardionetworks) for similar analyses in other cardiovascular diseases.

The Nrf2-ARE activation protect neurones against oxidative stress

Oxidative stress has been implicated in the pathogenesis of many neurodegenerative diseases including Alzheimer’s disease. The transcription factor, Nrf2 (nuclear factor E2-related factor 2) that binds to the antioxidant responsive element (ARE) activates a battery of genes encoding enzymes and factors essential for neuronal survival. We have investigated the hypothesis that a downstream product of cyclooxygenase(COX-2), 15-deoxy-delta (12, 14)-prostagland in J2 (15d-PGJ2) has protective effects by activating the Nrf2 pathway during oxidative stress.Human neuroblastoma cells (SHSY5Y) were differentiated intoneuronal-like cells as described previously (Gimenez-Cassina et al.,2006). SHSY5Y cells were co-treated with 10 mM buthionine sulfoximine (BSO) 7 10 mM 15d-PGJ2. Cell viability was measured by MTT assay and cellular glutathione (GSH) levels were measured after treating cells for0.5-24 hours by GSH recycling assay. Cellular Nrf2 levels were determined by immunoblotting. IL-6 levels were measured by ELISA.15d-PGJ2 alone lowered GSH levels 30min after the treatment(12.870.64 nmol/mg protein) and returned to untreated control levels at 16hours (28.173.6 nmol/mg protein; Po0.01). Compared to intracellular GSH levels in untreated cells (27.871.8 nmol/mg protein) BSO treatment alone significantly decreased GSH (9.672.1 nmol/mg protein;Po0.001) but co-incubation with 15d-PGJ2 for 24 hours prevented the depletion elicited by BSO(21.372.7 nmol/mg protein). Compared to untreated cells BSO treatment decrease dIL-6 secretion (from 0.941.6ng/ml to 0.6971.3ng/ml) and total Nrf2 protein levels (by21%). Co-incubation with15d-PGJ2 for 24 hours with BSO did not change IL-6(0.6771.4ng/ml) or total Nrf2 level at any time point. This study suggests that neuronal toxicity resulting from glutathione depletion canbere stored by the induction of Nrf2-ARE pathway and the role of the Nrf2 signalling merits further investigation in neurodegenerative diseases.

Hydrogen sulfide:a novel mechanism for the vascular protection by resveratrol under oxidative stress in mouse aorta

Reactive oxygen species (ROS) decreases bioavailability of nitric oxide (NO) and impairs NO-dependent relaxations. Like NO, hydrogen sulfide (H2S) is an antioxidant and vasodilator; however, the effect of ROS on H2S-induced relaxations is unknown. Here we investigated whether ROS altered the effect of H2S on vascular tone in mouse aorta and determined whether resveratrol (RVT) protects it via H2S. Pyrogallol induced ROS formation. It also decreased H2S formation and relaxation induced by l-cysteine and in mouse aorta. Pyrogallol did not alter sodium hydrogensulfide (NaHS)-induced relaxation suggesting that the pyrogallol effect on l-cysteine relaxations was due to endogenous H2S formation. RVT inhibited ROS formation, enhanced l-cysteine-induced relaxations and increased H2S level in aortas exposed to pyrogallol suggesting that RVT protects against "H2S-dysfunctions" by inducing H2S formation. Indeed, H2S synthesis inhibitor AOAA inhibited the protective effects of RVT. RVT had no effect on Ach-induced relaxation that is NO dependent and the stimulatory effect of RVT on H2S-dependent relaxation was also independent of NO. These results demonstrate that oxidative stress impairs endogenous H2S-induced relaxations and RVT offers protection by inducing H2S suggesting that targeting endogenous H2S pathway may prevent vascular dysfunctions associated by oxidative stress.