Learning the Silicon Valley Way" is the incremental process of firm-building and market-building that underlay the formation of the world's preeminent high-technology, high growth economy. Revisiting Moore's experiences as an early employee of Shockley Semiconductor and as a cofounder of Fairchild Semiconductor and Intel, we emphasize the necessary conditions for the takeoff of Silicon Valley. These conditions include broad-based learning of the many facets of managing commercial scientific endeavors-from managing internal incentives to limiting the dimensions of external competition-and the central importance of a large technological opportunity. At the same time, we reevaluate and downplay the role that military spending, university proximity, and central planning played in the evolution of this economy. The end result is an almost iconoclastic, and we believe, more accurate picture of the crucial elements in a nascent high-tech regional economy.

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Many bacteria use quorum sensing (QS) to regulate virulence factor production in response to changes in population density. QS is mediated through the production, secretion, and detection of signaling molecules called autoinducers (AIs) to modulate population-wide behavioral changes. Four histidine kinases, LuxPQ, CqsS, CqsR and VpsS, have been identified in Vibrio cholerae as QS receptors to activate virulence gene expression at low cell density. Detection of AIs by these receptors leads to virulence gene repression at high cell density. The redundancy among these receptors is puzzling since any one of the four receptors is sufficient to support colonization of V. cholerae in the host small intestine. It is believed that one of the functions of such circuit architecture is to prevent interference on any single QS receptor. However, it is unclear what natural molecules can interfere V. cholerae QS and in what environment interference is detrimental. We show here mutants expressing only CqsR without the other three QS receptors are defective in colonizing the host large intestine. We identified ethanolamine, a common intestinal metabolite that can function as a chemical source of QS interference. Ethanolamine specifically interacts with the ligand-binding CACHE domain of CqsR and induces a premature QS response in V. cholerae mutants expressing only CqsR without the other three QS receptors. The effect of ethanolamine on QS gene expression and host colonization is abolished by mutations that disrupt CqsR signal sensing. V. cholerae defective in producing ethanolamine is still proficient in QS, therefore, ethanolamine functions only as an external cue for CqsR. Our findings suggest the inhibitory effect of ethanolamine on CqsR could be a possible source of QS interference but is masked by the presence of the other parallel QS pathways, allowing V. cholerae to robustly colonize the host.

Data for this research were sourced from SIRCA (www.sirca.org.au). We are grateful to Ken Chapman of the ASX, Tamas Szabo of IG Markets, Cesario Mateus, and Gonul Colak for valuable comments on an earlier draft, to seminar participants at

This paper examines the impact of recent changes in the prudential regulation of non-bank financial institutions in Australia, with a particular focus upon the implications for coöperative financial institutions, such as credit unions. Such institutions are unable to raise external capital to satisfy regulatory capital requirements, and are thus forced to rely upon retained surpluses to generate capital. This, it is argued, creates an incompatibility between the regulatory structure and institutional form, imposes an arbitrary constraint on coöperatives' growth and can induce a focus upon inappropriate financial targets by credit union management. A further impediment to the survival of coöperative financial institutions can be found in the risk weights applied for capital adequacy purposes. It is suggested that these constraints will hasten the on-going decline in the number of credit unions through mergers and conversions to alternative forms.