The governance of formal university–industry interactions: understanding the rationales for alternative models

This article develops a conceptual framework to explain the economic rationale underpinning the choice of different modes of governance of formal university–industry interactions: personal contractual interactions, where the contract regulating the collaboration involves a firm and an individual academic researcher, and institutional interactions, where the relationship between the firm and the academic is mediated by the university. Although institutional interactions, for numerous reasons, have become more important, both governance modes are currently being implemented. We would argue that they have some important specificities that need to be understood if university–industry knowledge transfer is to be managed effectively and efficiently

Early Cretaceous absolute geomagnetic paleointensities from Córdoba province (Argentina)

We present here new paleointensity and geochronology results from Early Cretaceous volcanic rocks of Sierra Chica de Cordoba (Argentina). The new K-Ar isotopic ages of 5 samples range from 136 to 122 Ma. Twenty five samples from 7 individual flows yielded acceptable paleointensity estimates. The mean paleointensity values per flow are ranging from 53.0±1.9 to 25.4±2.6 μT and the corresponding Virtual Dipole Moments (VDMs) are ranging from 9.3±1.3 to 4.6±0.5 (1022 Am2). This corresponds to the mean value of 7.3±1.7x1022 Am2, which is compatible to the present geomagnetic axial dipole. Currently available selected paleointensity data from 80 to 130 Ma suggest that geomagnetic field strength frequently fluctuated before and during the Cretaceous Normal Superchron while the magnetic polarity maintained stable. The mean paleointensities derived from Cordoba lavas agree remarkably well with those obtained from the Parana Magmatic Province (133-132 Ma). This reinforces the hypothesis about the unreliability of ‘Mesozoic Dipole Low'.Fil: Cejudo Ruiz, Ruben. Universidad Nacional Autónoma de México; MéxicoFil: Goguitchaichvili, Avto. Universidad Nacional Autónoma de México; MéxicoFil: Geuna, Silvana Evangelina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Geociencias Básicas, Aplicadas y Ambientales de Buenos Aires. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Geociencias Básicas, Aplicadas y Ambientales de Buenos Aires; ArgentinaFil: Alva-Valdivia, Luis M.. Universidad Nacional Autónoma de México; MéxicoFil: Solé, Jesus. Universidad Nacional Autónoma de México; MéxicoFil: Morales, Juan. Universidad Nacional Autónoma de México; Méxic

IL-12 inhibition of endothelial cell functions and angiogenesis depends on lymphocyte-endothelial cell cross-talk.

In vivo IL-12-dependent tumor inhibition rests on the ability of IL-12 to activate a CD8-mediated cytotoxicity, inhibit angiogenesis, and cause vascular injury. Although in vivo studies have shown that such inhibition stems from complex interactions of immune cells and the production of IFN-gamma and other downstream angiostatic chemokines, the mechanisms involved are still poorly defined. Here we show that IL-12 activates an anti-angiogenic program in Con A-activated mouse spleen cells (activated spc) or human PBMC (activated PBMC). The soluble factors they release in its presence arrest the cycle of endothelial cells (EC), inhibit in vitro angiogenesis, negatively modulate the production of matrix metalloproteinase-9, and the ability of EC to adhere to vitronectin and up-regulate ICAM-1 and VCAM-1 expression. These effects do not require direct cell-cell contact, yet result from continuous interaction between activated lymphoid cells and EC. We used neutralizing Abs to show that the IFN-inducible protein-10 and monokine-induced by IFN-gamma chemokines are pivotal in inducing these effects. Experiments with nu/nu mice, nonobese diabetic-SCID mice, or activated spc enriched in specific cell subpopulations demonstrated that CD4(+), CD8(+), and NK cells are all needed to mediate the full anti-angiogenetic effect of IL-12