Nanotechnology, Industry Competitiveness and University Strategies: the Case of the UWS Nanotechnology Network in South-West Sydney

University-industry alliances have long been pursued by public funded programs hoping to boost innovation spillovers in a geographical or cognitive area of research-strength by universities. However, there is still a lack of industry-university cooperation in many fields while at the same time the benefits of universities to their regions’ knowledge intensity is firmly advocated (Acs 2004, Martinez-Fernandez & Leevers 2004, Martinez-Fernandez 2004)). The issue is not limited to the dissemination of knowledge, a traditional role of universities, but to introducing change into the region’s innovation system through activities that increase industry competitive advantage. Results from a project conducted in South-West Sydney from 2003 to 2005 shows that active industry engagement by Universities offering specific expertise in frontier technologies has a positive effect in university-industry cooperation if compared with other technologies well established in the private sector. The project results also show that the role of Universities as active facilitators of industry engagement in frontier technologies is a critical element in the regional/local innovation system where the university operates. The paper discusses first the context of the emergence of the UWS Nanotechnology Network as a sophisticated knowledge intensive service activity led by the University. Secondly the paper discusses the particular case of nanotechnology as a science in an early path and the role of universities at this particular stage. Thirdly, the paper discusses the use and barriers of firms to nanotechnology applications and the role played by UWS during the duration of the project. Finally policy issues arise in relation to the role of the public education sector in the early promotion of frontier technologies. References Acs, Z. (2002) Innovation and the Growth of Cities. Edward Elgar Publishing Ltd. Martinez-Fernandez, M.C. (2004) ‘Regional Collaboration Infrastructure: Effects in the Hunter Valley of NSW’, Australian Planner Vol 41(4); Planning Institute of Australia: Queensland. Martinez-Fernandez, M.C. and K. Leevers (2004) ‘Knowledge Creation, Sharing and Transfer as an Innovation Strategy: The Discovery of Nano-technology by South-West Sydney’. International Journal of Technology Management (IJTM), Volume 28 (3/4/5/6): 560-581.

Decreased Fetal Size Is Associated With β-Cell Hyperfunction in Early Life and Failure With Age

OBJECTIVE—Low birth weight is associated with diabetes in adult life. Accelerated or “catch-up” postnatal growth in response to small birth size is thought to presage disease years later. Whether adult disease is caused by intrauterine β-cell–specific programming or by altered metabolism associated with catch-up growth is unknown

Diet and Energy-Sensing Inputs Affect TorC1-Mediated Axon Misrouting but Not TorC2-Directed Synapse Growth in a Drosophila Model of Tuberous Sclerosis

The Target of Rapamycin (TOR) growth regulatory system is influenced by a number of different inputs, including growth factor signaling, nutrient availability, and cellular energy levels. While the effects of TOR on cell and organismal growth have been well characterized, this pathway also has profound effects on neural development and behavior. Hyperactivation of the TOR pathway by mutations in the upstream TOR inhibitors TSC1 (tuberous sclerosis complex 1) or TSC2 promotes benign tumors and neurological and behavioral deficits, a syndrome known as tuberous sclerosis (TS). In Drosophila, neuron-specific overexpression of Rheb, the direct downstream target inhibited by Tsc1/Tsc2, produced significant synapse overgrowth, axon misrouting, and phototaxis deficits. To understand how misregulation of Tor signaling affects neural and behavioral development, we examined the influence of growth factor, nutrient, and energy sensing inputs on these neurodevelopmental phenotypes. Neural expression of Pi3K, a principal mediator of growth factor inputs to Tor, caused synapse overgrowth similar to Rheb, but did not disrupt axon guidance or phototaxis. Dietary restriction rescued Rheb-mediated behavioral and axon guidance deficits, as did overexpression of AMPK, a component of the cellular energy sensing pathway, but neither was able to rescue synapse overgrowth. While axon guidance and behavioral phenotypes were affected by altering the function of a Tor complex 1 (TorC1) component, Raptor, or a TORC1 downstream element (S6k), synapse overgrowth was only suppressed by reducing the function of Tor complex 2 (TorC2) components (Rictor, Sin1). These findings demonstrate that different inputs to Tor signaling have distinct activities in nervous system development, and that Tor provides an important connection between nutrient-energy sensing systems and patterning of the nervous system

MAP4K3 Is a Component of the TORC1 Signalling Complex that Modulates Cell Growth and Viability in Drosophila melanogaster

Background: MAP4K3 is a conserved Ser/Thr kinase that has being found in connection with several signalling pathways, including the Imd, EGFR, TORC1 and JNK modules, in different organisms and experimental assays. We have analyzed the consequences of changing the levels of MAP4K3 expression in the development of the Drosophila wing, a convenient model system to characterize gene function during epithelial development. Methodology and Principal Findings: Using loss-of-function mutants and over-expression conditions we find that MAP4K3 activity affects cell growth and viability in the Drosophila wing. These requirements are related to the modulation of the TORC1 and JNK signalling pathways, and are best detected when the larvae grow in a medium with low protein concentration (TORC1) or are exposed to irradiation (JNK). We also show that MAP4K3 display strong genetic interactions with different components of the InR/Tor signalling pathway, and can interact directly with the GTPases RagA and RagC and with the multi-domain kinase Tor. Conclusions and Significance: We suggest that MAP4K3 has two independent functions during wing development, one related to the activation of the JNK pathway in response to stress and other in the assembling or activation of the TORC1 complex, being critical to modulate cellular responses to changes in nutrient availability

Pro-Survival Role for Parkinson's Associated Gene DJ-1 Revealed in Trophically Impaired Dopaminergic Neurons

A mouse genetic study reveals a novel cell-survival role for the Parkinson's disease-associated gene DJ-1 in dopaminergic neurons that have reduced support from endogenous survival factors

Dynamic Switch of Negative Feedback Regulation in Drosophila Akt–TOR Signaling

Akt represents a nodal point between the Insulin receptor and TOR signaling, and its activation by phosphorylation controls cell proliferation, cell size, and metabolism. The activity of Akt must be carefully balanced, as increased Akt signaling is frequently associated with cancer and as insufficient Akt signaling is linked to metabolic disease and diabetes mellitus. Using a genome-wide RNAi screen in Drosophila cells in culture, and in vivo analyses in the third instar wing imaginal disc, we studied the regulatory circuitries that define dAkt activation. We provide evidence that negative feedback regulation of dAkt occurs during normal Drosophila development in vivo. Whereas in cell culture dAkt is regulated by S6 Kinase (S6K)–dependent negative feedback, this feedback inhibition only plays a minor role in vivo. In contrast, dAkt activation under wild-type conditions is defined by feedback inhibition that depends on TOR Complex 1 (TORC1), but is S6K–independent. This feedback inhibition is switched from TORC1 to S6K only in the context of enhanced TORC1 activity, as triggered by mutations in tsc2. These results illustrate how the Akt–TOR pathway dynamically adapts the routing of negative feedback in response to the activity load of its signaling circuit in vivo

Lifespan Extension by Preserving Proliferative Homeostasis in Drosophila

Regenerative processes are critical to maintain tissue homeostasis in high-turnover tissues. At the same time, proliferation of stem and progenitor cells has to be carefully controlled to prevent hyper-proliferative diseases. Mechanisms that ensure this balance, thus promoting proliferative homeostasis, are expected to be critical for longevity in metazoans. The intestinal epithelium of Drosophila provides an accessible model in which to test this prediction. In aging flies, the intestinal epithelium degenerates due to over-proliferation of intestinal stem cells (ISCs) and mis-differentiation of ISC daughter cells, resulting in intestinal dysplasia. Here we show that conditions that impair tissue renewal lead to lifespan shortening, whereas genetic manipulations that improve proliferative homeostasis extend lifespan. These include reduced Insulin/IGF or Jun-N-terminal Kinase (JNK) signaling activities, as well as over-expression of stress-protective genes in somatic stem cell lineages. Interestingly, proliferative activity in aging intestinal epithelia correlates with longevity over a range of genotypes, with maximal lifespan when intestinal proliferation is reduced but not completely inhibited. Our results highlight the importance of the balance between regenerative processes and strategies to prevent hyperproliferative disorders and demonstrate that promoting proliferative homeostasis in aging metazoans is a viable strategy to extend lifespan

Integration of P2Y receptor-activated signal transduction pathways in G protein-dependent signalling networks

The role of nucleotides in intracellular energy provision and nucleic acid synthesis has been known for a long time. In the past decade, evidence has been presented that, in addition to these functions, nucleotides are also autocrine and paracrine messenger molecules that initiate and regulate a large number of biological processes. The actions of extracellular nucleotides are mediated by ionotropic P2X and metabotropic P2Y receptors, while hydrolysis by ecto-enzymes modulates the initial signal. An increasing number of studies have been performed to obtain information on the signal transduction pathways activated by nucleotide receptors. The development of specific and stable purinergic receptor agonists and antagonists with therapeutical potential largely contributed to the identification of receptors responsible for nucleotide-activated pathways. This article reviews the signal transduction pathways activated by P2Y receptors, the involved second messenger systems, GTPases and protein kinases, as well as recent findings concerning P2Y receptor signalling in C6 glioma cells. Besides vertical signal transduction, lateral cross-talks with pathways activated by other G protein-coupled receptors and growth factor receptors are discussed

Influences of non-singular stresses on plane-stress near-tip fields for pressure-sensitive materials and applications to transformation toughened ceramics

In this paper, we investigate the effects of the non-singular stress ( T stress) on the mode I near-tip fields for elastic perfectly plastic pressure-sensitive materials under plane-stress and small-scale yielding conditions. The T stress is the normal stress parallel to the crack faces. The yield criterion for pressure-sensitive materials is described by a linear combination of the effective stress and the hydrostatic stress. Plastic dilatancy is introduced by the normality flow rule. The results of our finite element computations based on a two-parameter boundary layer formulation show that the total angular span of the plastic sectors of the near-tip fields increases with increasing T stress for materials with moderately large pressure sensitivity. The T stress also has significant effects on the sizes and shapes of the plastic zones. The height of the plastic zone increases substantially as the T stress increases, especially for materials with large pressure sensitivity. When the plastic strains are considered to be finite as for transformation toughened ceramics, the results of our finite element computations indicate that the phase transformation zones for strong transformation ceramics with large pressure sensitivity can be approximated by those for elastic-plastic materials with no limit on plastic strains. When the T stress and the stress intensity factor K are prescribed in the two-parameter boundary layer formulation to simulate the crack-tip constraint condition for a single-edge notch bend specimen of zirconia ceramics, our finite element computation shows a spear shape of the phase transformation zone which agrees well with the corresponding experimental observation.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/42782/1/10704_2004_Article_BF00018779.pd

Possible phase transformation toughening of thermoset polymers by poly(butylene terephthalate)

Mechanisms were explored by which particles of poly(butylene terephthalate) (PBT) are able to toughen a brittle epoxy. The epoxy studied was an aromatic amine-cured diglycidyl ether of bisphenol-A, which was toughened at about twice the rate with particles of poly(butylene terephthalate) as with particles of nylon 6, poly(vinylidene fluoride), or CTBN rubber. Many of the mechanisms of toughening are visible on the fracture surface of the PBT-epoxy blend, but a mechanism suggested to account for perhaps half of the increased toughness with PBT, phase transformation toughening, is not. The two types of experiment performed to detect phase transformation toughening were: (1) measurements of the rubber cavitation zone in PBT-CTBN rubber-epoxy ternary blends, which would detect an expansion of the PBT particles during fracture if it occurred, and (2) measurements of the fracture energy in PBT-epoxy blends in which the various mechanisms of toughening were selectively suppressed. Both types of experiment indicated the occurrence of phase transformation toughening in these PBT-epoxy blends.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44711/1/10853_2005_Article_BF01154110.pd