Engineering of small-molecule gels based on the thermodynamics and kinetics of fiber formation

In this chapter, we will give an overview of our work on manipulating the micro/nano structure and macroscopic properties of SMGs. Firstly, it will cover the analysis of the thermodynamics of fiber formation in SMGs and the classification and characterization of the topological and micro/nano structures of fiber networks, followed by the analysis of the formation kinetics of these networks. The criteria of engineering of the SMGs will be summarized according to the latest understanding of the formation mechanisms of fiber networks. On the basis of this understanding, approaches that have been developed to engineer the micro/nanometer structures and macroscopic properties of typical SMGs will be presented.

Carbon nanotubes formed in graphite after mechanical grinding and thermal annealing

Multi-walled carbon nanotubes with cylindrical and bamboo-type structures are produced in a graphite sample after mechanical milling at ambient temperature and subsequent thermal annealing up to 1400 °C. The ball milling produces a precursor structure and the thermal annealing activates the nanotube growth. Different nanotubular structures indicate different formation mechanisms: multi-wall cylindrical carbon nanotubes are probably formed upon micropores and the bamboo tubes are produced because of the metal catalysts. A two-dimensional growth governed by surface diffusion is believed to be one important factor for the nanotube growth. A potential industrial production method is demonstrated with advantages of large production quantity and low cost.

Pure boron nitride nanowires produced from boron triiodide

A thick layer of pure boron nitride (BN) nanowires with a uniform diameter of 20 nm was synthesized for the first time using a CVD process with a new precursor of boron triiodide (BI3). Transmission electron microscopy revealed a nanocrystalline structure in the BN nanowires and the absence of any catalyst particle. Some BN nanowires self-assembled into thick threads up to several hundred micrometres long on top of the nanowire layer. The nitriding reactions and lack of catalyst suggest new formation mechanisms of the BN nanowires.

Characteristics of the deformed and recrystallised grains obtained after hot plane strain compression of a model Fe-30wt%Ni alloy

The development of physically-based models of microstructural evolution during hot deformation of metallic materials requires knowledge of the grain/subgrain structure and crystallographic texture characteristics over a range of processing conditions. A Fe-30wt%Ni based alloy, retaining a stable austenitic structure at room temperature, was used for modelling the development of austenite microstructure during hot deformation of conventional carbon-manganese steels. A series of plane strain compression tests was carried out at a temperature of 950 °C and strain rates of 10 s-1 and 0.1 s-1 to several strain levels. Evolution of the grain/subgrain structure and crystallographic texture was characterised in detail using quantitative light microscopy and highresolution electron backscatter diffraction. Crystallographic texture characteristics were determined separately for the observed deformed and recrystallised grains. The subgrain geometry and dimensions together with the misorientation vectors across sub-boundaries were quantified in detail across large sample areas and the orientation dependence of these characteristics was determined. Formation mechanisms of the recrystallised grains were established in relation to the deformation microstructure.

Formation of ultra-fine ferrite in hot rolled strip: potential mechanisms for grain refinement

A novel single-pass hot strip rolling process has been developed in which ultra-fine (<2 μm) ferrite grains form at the surface of hot rolled strip in two low carbon steels with average austenite grain sizes above 200 μm. Two experiments were performed on strip that had been re-heated to 1250°C for 300 s and air-cooled to the rolling temperatures. The first involved hot rolling a sample of 0.09 wt.%C–1.68Mn–0.22Si–0.27Mo steel (steel A) at 800°C, which was just above the Ar3 of this sample, while the second involved hot rolling a sample of 0.11C–1.68Mn–0.22Si steel (steel B) at 675°C, which is just below the Ar3 temperature of the sample. After air cooling, the surface regions of strip of both steel A and B consisted of ultra-fine ferrite grains which had formed within the large austenite grains, while the central regions consisted of a bainitic microstructure. In the case of steel B, a network of allotriomorphic ferrite delineated the prior-austenite grain boundaries throughout the strip cross-section. Based on results from optical microscopy and scanning/transmission electron microscopy, as well as bulk X-ray texture analysis and microtextural analysis using Electron Back-Scattered Diffraction (EBSD), it is shown that the ultra-fine ferrite most likely forms by a process of rapid intragranular nucleation during, or immediately after, deformation. This process of inducing intragranular nucleation of ferrite by deformation is referred to as strain-induced transformation.

New voice, same story? Social entrepreneurship and active social capital formation

The development of the third sector in Australia has involved the negotiation of varying forms of state and market regulatory mechanisms. In the course of these settlements, ground-up initiatives have often found that authenticity is only the starting point on journeys that end in incorporation. Social entrepreneurship is an emerging set of ideas which attempts to hold on to the authentic and unique elements generated by grassroots actions. What are its chances of success? This article sets out to answer this question through a discussion of regulation and social capital. A four-fold model of social cap ita I formation is advanced which outlines 'defensive', 'consolidative', 'inclusive' and 'regulated' social capital. It is concluded that while social entrepreneurship has the potential to shift social capital formation from reactive to active forms, it is likely to become increasingly standardised and regulated.

Development of the sheared edge in the trimming of steel and light metal sheet, part 2 - mechanisms and modelling

The shearing behavior of a drawing-steel and aluminum alloy were investigated using hardness contours of partially deformed samples and a finite element model of the trimming process. Results showed that the stress and strain distributions within the work-piece were more strongly dependent on the punch penetration than the material properties of the work-piece. Differences in the final fracture surface profile and burr formation of the drawing-steel and aluminum alloy were a consequence of the shape of the stress and strain distribution when the crack in the sample became unstable, not when it was initiated. Results and existing literature suggest that a correlation may exist between the strain-rate sensitivity of the work-piece material and the burr mechanism and fracture surface profile of the trimmed part.

Integrating insurance services, trust and risk mechanisms into multi-agent systems

In multi-agent systems, there is often the need for an agent to cooperate with others so as to ensure that a given task is achieved timely and cost effectively. Currently multi-agent systems maximize this through mechanisms such as coalition formation, trust and risk assessments, etc. In this paper, we incorporate the concept of insurance with trust and risk mechanisms in multi-agent systems. The novelty of this proposal is that it ensures continuous sharing of resources while encouraging expected utility to be maximized in a dynamic environment. Our experimental results confirm the feasibility of our approach.

Signaling mechanisms coupled to tyrosines in the granulocyte colony-stimulating factor receptor orchestrate G-CSF-induced expansion of myeloid progenitor cells

Granulocyte colony-stimulating factor (G-CSF) is the major regulator of neutrophil production. Studies in cell lines have established that conserved tyrosines Y704, Y729, Y744, Y764 within the cytoplasmic domain of G-CSF receptor (G-CSF-R) contribute significantly to G-CSF-induced proliferation, differentiation and cell survival. However, it is unclear whether these tyrosines are equally important under more physiological conditions. Here, we investigated how individual G-CSF-R tyrosines affect G-CSF responses of primary myeloid progenitors. We generated GCSF- R deficient mice and transduced their bone marrow cells with tyrosine "null" mutant (mO), single tyrosine "add back" mutants or wild type (WT) receptors. G-CSFinduced responses were determined in primary colony assays, serial replatings and suspension cultures. We show that removal of all tyrosines had no major influence on primary colony growth. However, adding back Y764 strongly enhanced proliferativeresponses, which was reverted by inhibition of ERK activitity. Y729, which we found to be associated with the suppressor of cytokine signaling, SOCS3, had a negative effect on colony formation. After repetitive replatings, the clonogenic capacities of cells expressing mO gradually dropped compared to WT. The presence of Y729, but also Y704 and Y744, both involved in activation of STAT3, further reduced replating
efficiencies. Conversely, Y764 greatly elevated the clonogenic abilities of myeloid progenitors, resulting in a >104–fold increase of colony forming cells over mO after the fifth replating. These findings suggest that tyrosines in the cytoplasmic domain of G-CSF-R, although dispensable for G-CSF-induced colony growth, recruit signaling mechanisms that regulate the maintenance and outgrowth of myeloid progenitor cells.

Pharmacokinetic mechanisms for reduced toxicity of irinotecan by coadministered Thalidomide

The clinical use of irinotecan (CPT-11) is hindered by dose-limiting diarrhea and myelosuppression. Recent clinical studies indicate that thalidomide, a known tumor necrosis factor-alpha inhibitor, ameliorated the toxicities induced by CPT-11. However, the mechanisms for this are unknown. This study aimed to investigate whether combination of thalidomide modulated the toxicities of CPT-11 using a rat model and the possible role of the altered pharmacokinetic component in the toxicity modulation using in vitro models. The toxicity model was constructed by treatment of healthy rats with CPT-11 at 60 mg/kg per day by intravenous (i.v.) injection. Body weight, acute and delayed-onset diarrhea, blood cell counts, and macroscopic and microscopic intestinal damages were monitored in rats treated with CPT-11 alone or combined therapy with thalidomide at 100 mg/kg administered by intraperitoneal (i.p.) injection. Single dose and 5-day multiple-dose studies were conducted in rats to examine the effects of concomitant thalidomide on the plasma pharmacokinetics of CPT-11 and its major metabolites SN-38 and SN-38 glucuronide (SN-38G). The effect of CPT-11 on thalidomide's pharmacokinetics was also checked. Rat liver microsomes and a rat hepatoma cell line, H4-II-E cells, were used to study the in vitro metabolic interactions between these two drugs. H4-II-E cells were also used to investigate the effect of thalidomide and its hydrolytic products on the transport of CPT-11 and SN-38. In addition, the effect of thalidomide and its hydrolytic products on rat plasma protein binding of CPT-11 and SN-38 was examined. Administration of CPT-11 by i.v. for 4 consecutive days to rats induced significant body weight loss, decrease in neutrophil and lymphocyte counts, severe acute- and delayed-onset diarrhea, and intestinal damages. These toxicities were alleviated when CPT-11 was combined with thalidomide. In both single-dose and 5-day multiple-dose pharmacokinetic study, coadministered thalidomide significantly increased the area under the plasma concentration-time curve (AUC) of CPT-11, but the AUC and elimination half-life (t(1/2)) of SN-38 were significantly decreased. However, CPT-11 did not significantly alter the pharmacokinetics of thalidomide. Thalidomide at 25 and 250 microM and its hydrolytic products at a total concentration of 10 microM had no significant effect on the plasma protein binding of CPT-11 and SN-38, except for that thalidomide at 250 microM caused a significant increase in the unbound fraction (f(u)) of CPT-11 by 6.7% (P < 0.05). The hydrolytic products of thalidomide (total concentration of 10 microM), but not thalidomide, significantly decreased CPT-11 hydrolysis by 16% in rat liver microsomes (P < 0.01). The formation of both SN-38 and SN-38G from CPT-11, SN-38 glucuronidation, or intracellular accumulation of both CPT-11 and SN-38 in H4-II-E cells followed Michaelis-Menten kinetics with the one-binding site model being the best fit for the kinetic data. Coincubation or 2-hr preincubation of thalidomide at 25 microM and 250 microM and its hydrolytic products at 10 microM did not show any significant effects on CPT-11 hydrolysis and SN-38 glucuronidation. However, preincubation of H4-II-E cells with thalidomide (250 microM), its hydrolytic products (total concentration of 10 microM), or phthaloyl glutamic acid (one major thalidomide hydrolytic product, 10 microM) significantly increased the intracellular accumulation of SN-38, but not CPT-11 (P < 0.01). The dose-limiting toxicities of CPT-11 were alleviated by combination with thalidomide in rats and the pharmacokinetic modulation by thalidomide may partially explain its antagonizing effects on the toxicities of CPT-11. The hydrolytic products of thalidomide, instead of the parental drug, modulated the hepatic hydrolysis of CPT-11 and intracellular accumulation of SN-38, probably contributing to the altered plasma pharmacokinetics of CPT-11 and SN-38. Further studies are needed to explore the role of both pharmacokinetics and pharmacodynamic components in the protective effect of thalidomide against the toxicities of CPT-11.

A descriptive model for the formation of ultrafine grained steels

This paper presents a descriptive model to explain the mechanisms involved in the development of ultrafine grained structure in steels through dynamic strain induced transformation. The model considers the microstructural evolution during and after deformation as well as the role of different process variables. A key factor is the competition between nucleation and growth, where it is shown that many potential nuclei can be lost under certain conditions leading to a mixed or coarser grain size.

Softening mechanisms in two duplex stainless steels deformed in hot torsion

The aim of the present work was to undertake a detailed investigation of the softening mechanisms during hot deformation of a 21Cr-10Ni-3Mo (steel A) and a 21Cr-8Ni-3Mo (steel B) austenite/ferrite duplex stainless steels containing about 60% and 30% of austenite, respectively. The steels were subjected to hot deformation in torsion performed at 900 ºC and 1200 ºC using a strain rate of 0.7 s-1 to several strain levels. Quantitative optical and transmission electron microscopy were used in the investigation. Austenite was observed to soften via dynamic recovery (DRV) and dynamic recrystallisation (DRX) accompanied by DRV for the deformation temperatures of 900 °C and 1200 °C, respectively, for the both steels studied. DRX of austenite largely occurred through strain-induced grain boundary migration, complemented by (multiple) twinning, and developed significantly faster in steel A than in steel B, indicating that considerably larger strains partitioned into austenite in the former steel during deformation at 1200 °C. The above softening mechanism was accompanied by the formation of DRX grains from subgrains along the austenite/ferrite interface and by large-scale subgrain coalescence. At 900°C, stressassisted phase transitions between austenite and ferrite were observed, characterised by dissolution of the primary austenite, formation of Widmanstätten secondary austenite and gradual globularisation of the microstructure with increasing strain. These processes appeared to be significantly more widespread in steel B. The softening mechanism within ferrite for the both steels studied was classified as “continuous DRX”, characterised by a gradual increase in misorientations between neighbouring subgrains with strain, for the both deformation temperatures.

A potential novel rapid screening NMR approach to boundary film formation at solid interfaces in contact with ionic liquids

The boundary films generated on a series of inorganic compounds, typical of native films on metal and ceramic surfaces, when exposed to various ionic liquids (ILs) based on the trihexyl(tetradecyl)phosphonium cation have been characterized using multinuclear solid-state NMR. The NMR results indicate that SiO₂ and Mg(OH)₂ interact strongly with the anion and cation of each IL through a mechanism of adsorption of the anion and subsequent close proximity of the cation in a surface double layer (as observed through ¹H−²⁹Si cross polarization experiments). In contrast, Al₂O₃, MgO, ZnO, and ZrO₂ appear less active, strongly suggesting the necessity of hydroxylated surface groups in order to enhance the generation of these interfacial films. Using solid-state NMR to characterize such interfaces not only has the potential to elucidate mechanisms of wear resistance and corrosion protection via ILs, but is also likely to allow their rapid screening for such durability applications.

Mechanisms involved in the renal responses to intravenous and renal artery infusions of noradrenaline in conscious dogs

1. The renal haemodynamic and glomerular filtration rate (G.F.R.) responses to intravenous and intrarenal infusions of noradrenaline were studied in conscious dogs, either with or without prior blockade of angiotensin II formation with teprotide.

2. Infusion noradrenaline by either route resulted in dose-related rises in plasma renin activity.

3. Pretreatment with teprotide reduced the rise in mean arterial pressure and abolished the rise in G.F.R. seen during intravenous infusions of noradrenaline (0.1, 0.2 and 0.4 microgram/kg . min). Noradrenaline also reduced filtration fraction more after teprotide pretreatment.

4. Renal blood flow rose and renal vascular resistance fell in response to I.V. noradrenaline infusions. This renal vasodilatation was unaffected by pretreatment of the dogs with teprotide, indomethacin or DL-propranolol. However after pentolinium pretreatment, I.V. noradrenaline infusion caused a dose-related renal vasoconstriction.

5. Infusion of noradrenaline into the renal artery (0.02, 0.05 and 0.1 microgram/kg . min) resulted in rises in mean arterial pressure and G.F.R. which were abolished by teprotide pretreatment. Filtration fraction rose when noradrenaline was administered alone but fell when it was infused after teprotide treatment.

6. Thus angiotensin II formed as the result of increased renin release acted to maintain G.F.R. and filtration fraction during noradrenaline infusion. In addition, I.V. noradrenaline infusions in conscious dogs caused reflex vasodilatation of the renal vasculature.