Shear tests of rivet fastened rectangular hollow flange channel beams

The intermittently rivet fastened Rectangular Hollow Flange Channel Beam (RHFCB) is a new cold-formed hollow section proposed as an alternative to welded hollow flange channel beams. It is a monosymmetric channel section made by intermittently rivet fastening two torsionally rigid rectangular hollow flanges to a web plate. This process enables the end users to choose an effective combination of different web and flange plate sizes to achieve optimum design capacities. Recent research studies focused mainly on the shear behaviour of the most commonly used lipped channel beam and welded hollow flange beam sections. However, the shear behaviour of rivet fastened RHFCB has not been investigated. Therefore a detailed experimental study involving 24 shear tests was undertaken to investigate the shear behaviour and capacities of rivet fastened RHFCBs. Simply supported test specimens of RHFCB with aspect ratios of 1.0 and 1.5 were loaded at mid-span until failure. Comparison of experimental shear capacities with corresponding predictions from the current Australian cold-formed steel design rules showed that the current design rules are very conservative for the shear design of rivet fastened RHFCBs. Significant improvements to web shear buckling occurred due to the presence of rectangular hollow flanges while considerable post-buckling strength was also observed. Such enhancements to the shear behaviour and capacity were achieved with a rivet spacing of 100 mm. Improved design rules were proposed for rivet fastened RHFCBs based on the current shear design equations in AISI S100 and the direct strength method. This paper presents the details of this experimental investigation and the results.

Numerical modelling of rivet fastened rectangular hollow flange channel beams subject to shear

The intermittently rivet fastened Rectangular Hollow Flange Channel Beam (RHFCB) is a new cold-formed hollow section proposed as an alternative to welded hollow flange beams. Many experimental and numerical studies have been carried out in the past to investigate the shear behaviour of lipped channel beams. However, no research has been undertaken on the shear behaviour of rivet fastened RHFCBs. Therefore experimental and numerical studies were undertaken to investigate the shear behaviour and strength of rivet fastened RHFCBs. In this research finite element models of rivet fastened RHFCBs were developed to investigate their nonlinear shear behaviour including their buckling characteristics and ultimate shear strength. This paper presents the details of the finite element models of rivet fastened RHFCBs and the results. Both finite element analysis and experimental results showed that the current design rules are very conservative for the shear design of rivet fastened RHFCBs. Appropriate improvements have been proposed for the design rules of shear strength of rivet fastened RHFCBs within the Direct Strength Method format.

Shear tests of rivet fastened rectangular hollow flange channel beams with web openings

The rivet-fastened rectangular hollow flange channel beam (RHFCB) is a new cold-formed hollow section proposed as an alternative to welded hollow flange steel beams. No research has been undertaken on the shear behaviour and strength of rivet fastened RHFCBs with web openings. Hence a detailed experimental study involving 30 shear tests was undertaken to investigate the shear behaviour and strength of rivet fastened RHFCBs with web openings. Experimental results showed that the current design rules are inadequate for the shear design of Rivet fastened RHFCBs with web openings. Improved design equations have been proposed for the shear strength of rivet fastened RHFCBs with web openings.

Stress and developmental responses in Arabidopsis thaliana: regulation through the transcription factor-interacting protein RCD1

Plants constantly face adverse environmental conditions, such as drought or extreme temperatures that threaten their survival. They demonstrate astonishing metabolic flexibility in overcoming these challenges and one of the key responses to stresses is changes in gene expression leading to alterations in cellular functions. This is brought about by an intricate network of transcription factors and associated regulatory proteins. Protein-protein interactions and post-translational modifications are important steps in this control system along with carefully regulated degradation of signaling proteins. This work concentrates on the RADICAL-INDUCED CELL DEATH1 (RCD1) protein which is an important regulator of abiotic stress-related and developmental responses in Arabidopsis thaliana. Plants lacking this protein function display pleiotropic phenotypes including sensitivity to apoplastic reactive oxygen species (ROS) and salt, ultraviolet B (UV-B) and paraquat tolerance, early flowering and senescence. Additionally, the mutant plants overproduce nitric oxide, have alterations in their responses to several plant hormones and perturbations in gene expression profiles. The RCD1 gene is transcriptionally unresponsive to environmental signals and the regulation of the protein function is likely to happen post-translationally. RCD1 belongs to a small protein family and, together with its closest homolog SRO1, contains three distinguishable domains: In the N-terminus, there is a WWE domain followed by a poly(ADP-ribose) polymerase-like domain which, despite sequence conservation, does not seem to be functional. The C-terminus of RCD1 contains a novel domain called RST. It is present in RCD1-like proteins throughout the plant kingdom and is able to mediate physical interactions with multiple transcription factors. In conclusion, RCD1 is a key point of signal integration that links ROS-mediated cues to transcriptional regulation by yet unidentified means, which are likely to include post-translational mechanisms. The identification of RCD1-interacting transcription factors, most of whose functions are still unknown, opens new avenues for studies on plant stress as well as developmental responses.

Growth factor-loaded microparticles for tissue engineering: The discrepancies of in vitro characterization assays

Efficient and effective growth factor (GF) delivery is an ongoing challenge for tissue regeneration therapies. The accurate quantification of complex molecules such as GFs, encapsulated in polymeric delivery devices, is equally critical and just as complex as achieving efficient delivery of active GFs. In this study, GFs relevant to bone tissue formation, vascular endothelial growth factor (VEGF) and bone morphogenetic protein 7 (BMP-7), were encapsulated, using the technique of electrospraying, into poly(lactic-co-glycolic acid) microparticles that contained poly(ethylene glycol) and trehalose to assist GF bioactivity. Typical quantification procedures, such as extraction and release assays using saline buffer, generated a significant degree of GF interactions, which impaired accurate assessment by enzyme-linked immunosorbent assay (ELISA). When both dry BMP-7 and VEGF were processed with chloroform, as is the case during the electrospraying process, reduced concentrations of the GFs were detected by ELISA; however, the biological effect on myoblast cells (C2C12) or endothelial cells (HUVECs) was unaffected. When electrosprayed particles containing BMP-7 were cultured with preosteoblasts (MC3T3-E1), significant cell differentiation into osteoblasts was observed up to 3 weeks in culture, as assessed by measuring alkaline phosphatase. In conclusion, this study showed how electrosprayed microparticles ensured efficient delivery of fully active GFs relevant to bone tissue engineering. Critically, it also highlights major discrepancies in quantifying GFs in polymeric microparticle systems when comparing ELISA with cell-based assays.

Death pathways activated in the neurotrophic factor-deprived neurons

Programed cell death (PCD) is a fundamental biological process that is as essential for the development and tissue homeostasis as cell proliferation, differentiation and adaptation. The main mode of PCD - apoptosis - occurs via specifi c pathways, such as mitochondrial or death receptor pathway. In the developing nervous system, programed death broadly occurs, mainly triggered by the defi ciency of different survival-promoting neurotrophic factors, but the respective death pathways are poorly studied. In one of the best-characterized models, sympathetic neurons deprived of nerve growth factor (NGF) die via the classical mitochondrial apoptotic pathway. The main aim of this study was to describe the death programs activated in these and other neuronal populations by using neuronal cultures deprived of other neurotrophic factors. First, this study showed that the cultured sympathetic neurons deprived of glial cell line-derived neurotrophic factor (GDNF) die via a novel non-classical death pathway, in which mitochondria and death receptors are not involved. Indeed, cytochrome c was not released into the cytosol, Bax, caspase-9, and caspase-3 were not involved, and Bcl-xL overexpression did not prevent the death. This pathway involved activation of mixed lineage kinases and c-jun, and crucially requires caspase-2 and -7. Second, it was shown that deprivation of neurotrophin-3 (NT-3) from cultured sensory neurons of the dorsal root ganglia kills them via a dependence receptor pathway, including cleavage of the NT- 3 receptor TrkC and liberation of a pro-apoptotic dependence domain. Indeed, death of NT-3-deprived neurons was blocked by a dominant-negative construct interfering with TrkC cleavage. Also, the uncleavable mutant of TrkC, replacing the siRNA-silenced endogeneous TrkC, was not able to trigger death upon NT-3 removal. Such a pathway was not activated in another subpopulation of sensory neurons deprived of NGF. Third, it was shown that cultured midbrain dopaminergic neurons deprived of GDNF or brainderived neurotrophic factor (BDNF) kills them by still a different pathway, in which death receptors and caspases, but not mitochondria, are activated. Indeed, cytochrome c was not released into the cytosol, Bax was not activated, and Bcl-xL did not block the death, but caspases were necessary for the death of these neurons. Blocking the components of the death receptor pathway - caspase-8, FADD, or Fas - blocked the death, whereas activation of Fas accelerated it. The activity of Fas in the dopaminergic neurons could be controlled by the apoptosis inhibitory molecule FAIML. For these studies we developed a novel assay to study apoptosis in the transfected dopaminergic neurons. Thus, a novel death pathway, characteristic for the dopaminergic neurons was described. The study suggests death receptors as possible targets for the treatment of Parkinson s disease, which is caused by the degeneration of dopaminergic neurons.

Factor five - Towards global sustainability through doing much more with much less

This is a revised text of the third lecture of the 2014 public lecture series, "The Path Toward a Global Civilzation" hosted by the Institute of Oriental Philosophy on October 2 in Tokyo. Dr Desha is a research principal of the Australian team at the Natural Edge Project which published Factor 5: Transforming the Global Economy through 80% Increase in Resource Productivity (2009) in collaboration with Dr Ernst Ulrich von Weizsacker.

On the hardness of shear bands in amorphous alloys

The nanoindentation hardness of individual shear bands in a Zr-based metallic glass was investigated in order to obtain a better understanding of how shear band plasticity is influenced by non-crystalline defects. The results clearly showed that the shear band hardness in both as-cast and structurally relaxed samples is much lower than the respective hardness of undeformed region. Interestingly, inter-band matrix also exhibited lower hardness than undeformed region. The results are discussed in terms of the influence of structural state and the prevailing mechanism of plastic deformation.

Transition of turbulent pipe flow

The velocity profile in turbulent pipe flow is usually divided into two regions, a wall or inner region and a core or outer region. For the inner region, the viscosity and wall shear stress are the important parameters governing the velocity distribution whereas for the outer region, the wall reduces the velocity below the maximum velocity independent of viscosity. In the present work, a velocity model is proposed for turbulent flow in the wall region of a pipe covering the entire transition from smooth to rough flows. Coupling this model for the wall region with the power law velocity model for the core region, an equation for the friction factor is obtained. The model constants are evaluated by using Nikuradse's experiments in the fully smooth and rough turbulent flows. The model shows good agreement with the friction factor and the velocity profiles obtained by Nikuradse for the transition region of turbulent flow.

Spontaneous and reversible self-assembly of a polypeptide fragment of insulin-like growth factor binding protein-2 into fluorescent nanotubular structures

In this communication, we report the spontaneous and reversible in vitro self-assembly of a polypeptide fragment derived from the C-terminal domain of Insulin-like Growth Factor Binding Protein (IGFBP-2) into soluble nanotubular structures several micrometres long via a mechanism involving inter-molecular disulfide bonds and exhibiting enhanced fluorescence.

Transforming growth factor -beta signaling through Smad3 in allergy : Studies in the mechanisms of asthma, atopic dermatitis and allergic contact reactions

Transforming growth factor β signalling through Smad3 in allergy Allergic diseases, such as atopic dermatitis, asthma, and contact dermatitis are complex diseases influenced by both genetic and environmental factors. It is still unclear why allergy and subsequent allergic disease occur in some individuals but not in others. Transforming growth factor (TGF)-β is an important immunomodulatory and fibrogenic factor that regulates cellular processes in injured and inflamed skin. TGF-β has a significant role in the regulation of the allergen-induced immune response participating in the development of allergic and asthmatic inflammation. TGF-β is known to be an immunomodulatory factor in the progression of delayed type hypersensitivity reactions and allergic contact dermatitis. TGF-β is crucial in regulating the cellular responses involved in allergy, such as differentiation, proliferation and migration. TGF-β signals are delivered from the cytoplasm to the nucleus by TGF-β signal transducers called Smads. Smad3 is a major signal transducer in TGF-β -signalling that controls the expression of target genes in the nucleus in a cell-type specific manner. The role of TGF-β-Smad3 -signalling in the immunoregulation and pathophysiology of allergic disorders is still poorly understood. In this thesis, the role of TGF-β-Smad -signalling pathway using Smad3 -deficient knock out mice in the murine models of allergic diseases; atopic dermatitis, asthma and allergic contact reactions, was examined. Smad3-pathway regulates allergen induced skin inflammation and systemic IgE antibody production in a murine model atopic dermatitis. The defect in Smad3 -signalling decreased Th2 cytokine (IL-13 and IL-5) mRNA expression in the lung, modulated allergen induced specific IgG1 response, and affected mucus production in the lung in a murine model of asthma. TGF-β / Smad3 -signalling contributed to inflammatory hypersensitivity reactions and disease progression via modulation of chemokine and cytokine expression and inflammatory cell recruitment, cell proliferation and regulation of the specific antibody response in a murine model of contact hypersensitivity. TGF-β modulates inflammatory responses - at least partly through the Smad3 pathway - but also through other compensatory, non-Smad-dependent pathways. Understanding the effects of the TGF-β signalling pathway in the immune system and in disease models can help in elucidating the multilevel effects of TGF-β. Unravelling the mechanisms of Smad3 may open new possibilities for treating and preventing allergic responses, which may lead to severe illness and loss of work ability. In the future the Smad3 signalling pathway might be a potential target in the therapy of allergic diseases.