The effect of nickel on the martensitic-type transformations Of Pt3Al and TiPt

The effect of nickel on two classes of martensitic-type transformations in platinum systems has been studied. The first transformation is Ll2 to DO'c in the Pt3Al system and the second is B2 to B19 in the TiPt system. The microstructures after transformation in the two systems are very different. The product of the Pt3Al transformation has a twinned microstructure, typical of cubic-to-tetragonal transformations. The product of the TiPt transformation is lath-like, although the morphology can be altered using heat treatments. The parent phase in the TiPt system is not retained at room temperature, whereas the parent phase in the Pt3Al transformation can be stabilised to room temperature. A great variation in hardness and transformation temperature is seen in each system as the composition is varied about the stoichiometric ratio, which has the lowest hardness. The Pt3Al transformation temperature has been reported to range from around room temperature to 1000°C. The TiPt transformation temperature can range from 1000 to 1080°C. The effect of nickel additions on these alloys also has a marked effect on the parent and product phase stability, and hence the microstructure and resulting hardness. The effect on the Pt3Al phase is complex, as nickel appears to stabilise the parent phase. The hardness varied in the region of 350 to 500 HV10. For the TiPt phase, the hardness values were generally found to increase with the nickel additions increasing from 250 to about 600 HV10. The addition of 20 at.% nickel decreases the transformation temperature from around 1000°C to about 600°C

Revised phase diagram for the Pt-Ti system from 30 to 60 at.% platinum

Alloys of the Ti-Pt system between 30 and 61 at.% Pt were studied using metallography with optical and scanning electron microscopy (SEM), X-ray diffraction (XRD), and differential thermal analysis (DTA). A phase of nominal composition Ti4Pt3, in the range 41.7-43.4 at.% Pt was found in samples containing between 30 and 47 at.% Pt, and was apparently formed by a peritectoid reaction between β-TiPt and Ti3Pt at 1205±10°C. The eutectic reaction between Ti3Pt and β-TiPt was found to be at ∼35 at.% Pt and 1424±10°C, and the Ti3Pt phase melted at circa 1500°C. The other phase boundaries agreed with the published literature, except that a slightly wider range was found at 1200°C for β-TiPt. © 2004 Elsevier B.V. All rights reserved

Ovine pedomics : the first study of the ovine foot 16S rRNA-based microbiome

We report the first study of the bacterial microbiome of ovine interdigital skin based on 16S rRNA by pyrosequencing and conventional cloning with Sanger-sequencing. Three flocks were selected, one a flock with no signs of footrot or interdigital dermatitis, a second flock with interdigital dermatitis alone and a third flock with both interdigital dermatitis and footrot. The sheep were classified as having either healthy interdigital skin (H), interdigital dermatitis (ID) or virulent footrot (VFR). The ovine interdigital skin bacterial community varied significantly by flock and clinical condition. The diversity and richness of operational taxonomic units was greater in tissue from sheep with ID than H or VFR affected sheep. Actinobacteria, Bacteriodetes, Firmicutes and Proteobacteria were the most abundant phyla comprising 25 genera. Peptostreptococcus, Corynebacterium and Staphylococcus were associated with H, ID and VFR respectively. Sequences of Dichelobacter nodosus, the causal agent of ovine footrot, were not amplified due to mismatches in the 16S rRNA universal forward primer (27F). A specific real time PCR assay was used to demonstrate the presence of D. nodosus which was detected in all samples including the flock with no signs of ID or VFR. Sheep with ID had significantly higher numbers of D. nodosus (104-109 cells/g tissue) than those with H or VFR feet

Sites of persistence of Fusobacterium necrophorum and Dichelobacter nodosus: a paradigm shift in understanding the epidemiology of footrot in sheep

Sites of persistence of bacterial pathogens contribute to disease dynamics of bacterial diseases. Footrot is a globally important bacterial disease that reduces health and productivity of sheep. It is caused by Dichelobacter nodosus, a pathogen apparently highly specialised for feet, while Fusobacterium necrophorum, a secondary pathogen in footrot is reportedly ubiquitous on pasture. Two prospective longitudinal studies were conducted to investigate the persistence of D. nodosus and F. necrophorum in sheep feet, mouths and faeces, and in soil. Molecular tools were used to detect species, strains and communities. In contrast to the existing paradigm, F. necrophorum persisted on footrot diseased feet, and in mouths and faeces; different strains were detected in feet and mouths. D. nodosus persisted in soil and on diseased, but not healthy, feet; similar strains were detected on both healthy and diseased feet of diseased sheep. We conclude that D. nodosus and F. necrophorum depend on sheep for persistence but use different strategies to persist and spread between sheep within and between flocks. Elimination of F. necrophorum would be challenging due to faecal shedding. In contrast D. nodosus could be eliminated if all footrot-affected sheep were removed and fade out of D. nodosus occurred in the environment before re-infection of a foot

A distinct bacterial dysbiosis associated skin inflammation in ovine footrot

Ovine footrot is a highly prevalent bacterial disease caused by Dichelobacter nodosus and characterised by the separation of the hoof horn from the underlying skin. The role of innate immune molecules and other bacterial communities in the development of footrot lesions remains unclear. This study shows a significant association between the high expression of IL1β and high D. nodosus load in footrot samples. Investigation of the microbial population identified distinct bacterial populations in the different disease stages and also depending on the level of inflammation. Treponema (34%), Mycoplasma (29%) and Porphyromonas (15%) were the most abundant genera associated with high levels of inflammation in footrot. In contrast, Acinetobacter (25%), Corynebacteria (17%) and Flavobacterium (17%) were the most abundant genera associated with high levels of inflammation in healthy feet. This demonstrates for the first time there is a distinct microbial community associated with footrot and high cytokine expression

Pathoadaptive mutations of Escherichia coli K1 in experimental neonatal systemic infection

Although Escherichia coli K1 strains are benign commensals in adults, their acquisition at birth by the newborn may result in life-threatening systemic infections, most commonly sepsis and meningitis. Key features of these infections, including stable gastrointestinal (GI) colonization and age-dependent invasion of the bloodstream, can be replicated in the neonatal rat. We previously increased the capacity of a septicemia isolate of E. coli K1 to elicit systemic infection following colonization of the small intestine by serial passage through two-day-old (P2) rat pups. The passaged strain, A192PP (belonging to sequence type 95), induces lethal infection in all pups fed 2–6 x 106 CFU. Here we use whole-genome sequencing to identify mutations responsible for the threefold increase in lethality between the initial clinical isolate and the passaged derivative. Only four single nucleotide polymorphisms (SNPs), in genes (gloB, yjgV, tdcE) or promoters (thrA) involved in metabolic functions, were found: no changes were detected in genes encoding virulence determinants associated with the invasive potential of E. coli K1. The passaged strain differed in carbon source utilization in comparison to the clinical isolate, most notably its inability to metabolize glucose for growth. Deletion of each of the four genes from the E. coli A192PP chromosome altered the proteome, reduced the number of colonizing bacteria in the small intestine and increased the number of P2 survivors. This work indicates that changes in metabolic potential lead to increased colonization of the neonatal GI tract, increasing the potential for translocation across the GI epithelium into the systemic circulation

Platinum Alloys for Shape Memory Applications

Shape memory alloys (SMAs) are materials that can change their shape at a specific temperature and are used in applications as diverse as sensors, temperature sensitive switches, force actuators, fire-safety valves, orthodontic wires, fasteners, and couplers. The possible advantages offered by platinum-based SMAs involving the metals: iron, aluminium, gallium, titanium, chromium, and vanadium, are considered here and the likely systems upon which such alloys might be based are assessed. It is suggested that the most promising candidate systems are ternary-alloyed variations of the Pt 3Al and PtTi phases, although SMAs based on PtFe3 have potential for low temperature applications. It appears possible to engineer a shape memory transition in the (Pt, Ni)Ti system anywhere between room temperature and 1000°C, a versatility which is probably unique among all known SMAs

Non-invasive three-dimensional imaging of Escherichia coli K1 infection using diffuse light imaging tomography combined with micro-computed tomography

In contrast to two-dimensional bioluminescence imaging, three dimensional diffuse light imaging tomography with integrated micro-computed tomography (DLIT-μCT) has the potential to realise spatial variations in infection patterns when imaging experimental animals dosed with derivatives of virulent bacteria carrying bioluminescent reporter genes such as the lux operon from the bacterium Photorhabdus luminescens. The method provides an opportunity to precisely localise the bacterial infection sites within the animal and enables the generation of four-dimensional movies of the infection cycle. Here, we describe the use of the PerkinElmer IVIS SpectrumCT in vivo imaging system to investigate progression of lethal systemic infection in neonatal rats following colonisation of the gastrointestinal tract with the neonatal pathogen Escherichia coli K1. We confirm previous observations that these bacteria stably colonize the colon and small intestine following feeding of the infectious dose from a micropipette; invading bacteria migrate across the gut epithelium into the blood circulation and establish foci of infection in major organs, including the brain. DLIT-μCT revealed novel multiple sites of colonisation within the alimentary canal, including the tongue, oesophagus and stomach, with penetration of the non-keratinised oesophageal epithelial surface, providing strong evidence of a further major site for bacterial dissemination. We highlight technical issues associated with imaging of infections in new born rat pups and show that the whole-body and organ bioburden correlates with disease severity

Bioluminescent Imaging Reveals Novel Patterns of Colonization and Invasion in Systemic Escherichia coli K1 Experimental Infection in the Neonatal Rat

Key features of Escherichia coli K1-mediated neonatal sepsis and meningitis, such as a strong age dependency and development along the gut-mesentery-blood-brain course of infection, can be replicated in the newborn rat. We examined temporal and spatial aspects of E. coli K1 infection following initiation of gastrointestinal colonization in 2-day-old (P2) rats after oral administration of E. coli K1 strain A192PP and a virulent bioluminescent derivative, E. coli A192PP-lux2. A combination of bacterial enumeration in the major organs, two-dimensional bioluminescence imaging, and three-dimensional diffuse light imaging tomography with integrated micro-computed tomography indicated multiple sites of colonization within the alimentary canal; these included the tongue, esophagus, and stomach in addition to the small intestine and colon. After invasion of the blood compartment, the bacteria entered the central nervous system, with restricted colonization of the brain, and also invaded the major organs, in line with increases in the severity of symptoms of infection. Both keratinized and nonkeratinized surfaces of esophagi were colonized to a considerably greater extent in susceptible P2 neonates than in corresponding tissues from infection-resistant 9-day-old rat pups; the bacteria appeared to damage and penetrate the nonkeratinized esophageal epithelium of infection-susceptible P2 animals, suggesting the esophagus represents a portal of entry for E. coli K1 into the systemic circulation. Thus, multimodality imaging of experimental systemic infections in real time indicates complex dynamic patterns of colonization and dissemination that provide new insights into the E. coli K1 infection of the neonatal rat

A longitudinal study of the role of Dichelobacter nodosus and Fusobacterium necrophorum load in initiation and severity of footrot in sheep

Footrot is an infectious bacterial disease of sheep that causes lameness. The causal agent is Dichelobacter nodosus. There is debate regarding the role of Fusobacterium necrophorum in disease initiation. This research used an observational longitudinal study of footrot, together with quantitative PCR (qPCR) of bacterial load of D. nodosus and F. necrophorum, to elucidate the roles of each species in the development of disease. All feet of 18 a priori selected sheep were monitored for five weeks assessing disease severity (healthy, interdigital dermatitis (ID) and severe footrot (SFR)) and bacterial load. A multinomial model was used to analyse these data. Key results were that D. nodosus was detected more frequently on feet with ID, whereas F. necrophorum was detected more frequently on feet with SFR. In the multinomial model, ID was associated with increasing log10 load of D. nodosus the week of observation (OR = 1.28 (95% CI = 1.08-1.53)) and the week prior to development of ID (OR = 1.20 (95% CI = 1.01-1.42). There was no association between log10 load^2 of F. necrophorum and presence of ID (OR = 0.99 (95% CI = 0.96-1.02))). SFR was associated with increasing log10 load of D. nodosus the week before disease onset (OR = 1.42 (95% CI = 1.02-1.96)) but not once SFR had occurred. SFR was positively associated with log10 load^2 of F. necrophorum once disease was present (OR = 1.06 (95% CI = 1.01-1.11)). In summary, there was an increased risk of increasing D. nodosus load the week prior to development of ID and SFR and during an episode of ID. In contrast, F. necrophorum load was not associated with ID before or during an episode, and was only associated with SFR once present. These results contribute to our understanding of the epidemiology of footrot and highlight that D. nodosus load plays the primary role in disease initiation and progression, with F. necrophorum load playing a secondary role. Further studies in more flocks and climates would be useful to confirm these findings. This study identifies that D. nodosus load is highest during ID. This supports previous epidemiological findings, which demonstrate that controlling ID is the most effective management strategy to prevent new cases of ID and SFR