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Economic trends and a changing job market for college graduates have generated significant interest in graduating more engineers who possess entrepreneurship skills and an entrepreneurial mindset. This has led to significant growth in the delivery of entrepreneurship courses to engineering students; however, research shows that such courses are typically not part of the core engineering curriculum. The Accreditation Board for Engineering and Technology (ABET) establishes criteria for accrediting engineering programs and is a significant force in shaping the undergraduate curriculum. The purpose of this paper is to explore how an alignment of entrepreneurship education outcomes and ABET Criterion 3a-k3a-k, could catalyze the integration of the entrepreneurial skills and knowledge into engineering courses. Potential benefits of such an approach are the enhancement of mechanisms associated with achieving ABET accreditation while developing the entrepreneurial skills of engineering students.

. Sodium channel kinetic changes that produce Brugada syndrome or progressive cardiac conduction system disease. Am J Physiol Heart Circ Physiol 292: H399 -H407, 2007. First published July 28, 2006; doi:10.1152/ajpheart.01025.2005.-Some mutations of the sodium channel gene NaV1.5 are multifunctional, causing combinations of LQTS, Brugada syndrome and progressive cardiac conduction system disease (PCCD). The combination of Brugada syndrome and PCCD is uncommon, although they both result from a reduction in the sodium current. We hypothesize that slow conduction is sufficient to cause S-T segment elevation and undertook a combined experimental and theoretical study to determine whether conduction slowing alone can produce the Brugada phenotype. Deletion of lysine 1479 in one of two positively charged clusters in the III/IV inter-domain linker causes both syndromes. We have examined the functional effects of this mutation using heterologous expression of the wild-type and mutant sodium channel in HEK-293-EBNA cells. We show that ⌬K1479 shifts the potential of half-activation, V1/2m, to more positive potentials (V1/2m ϭ Ϫ36.8 Ϯ 0.8 and Ϫ24.5 Ϯ 1.3 mV for the wild-type and ⌬K1479 mutant respectively, n ϭ 11, 10). The depolarizing shift increases the extent of depolarization required for activation. The potential of half-inactivation, V1/2h, is also shifted to more positive potentials (V1/2h ϭ Ϫ85 Ϯ 1.1 and Ϫ79.4 Ϯ 1.2 mV for wild-type and ⌬K1479 mutant respectively), increasing the fraction of channels available for activation. These shifts are quantitatively the same as a mutation that produces PCCD only, G514C. We incorporated experimentally derived parameters into a model of the cardiac action potential and its propagation in a one dimensional cable (simulating endo-, mid-myocardial and epicardial regions). The simulations show that action potential and ECG changes consistent with Brugada syndrome may result from conduction slowing alone; marked repolarization heterogeneity is not required. The findings also suggest how Brugada syndrome and PCCD which both result from loss of sodium channel function are sometimes present alone and at other times in combination. sodium channel; Brugada syndrome; conduction system disease PROGRESSIVE CARDIAC CONDUCTION SYSTEM DISEASE (PCCD) and a subset of Brugada syndrome are allelic disorders. They may result from mutations in the ␣-subunit of the cardiac sodium channel gene, Na V1.5 . The fundamental defect that may produce both syndromes falls into the following two categories 1) synthesis of a nonfunctional protein or failure of membrane insertion of the synthesized protein or 2) changes in channel kinetics that reduce the inward sodium current during phases 0 and 1 of the action potential (3,21,27). In a subset of patients with Brugada syndrome, reduction of the sodium current during late phase 0 and early phase 1 shifts the action potential current-voltage trajectory in the outward direction. This exaggerates the normal epicardial to endocardial repolarization gradient that ...

These direct data are the first to support the hypothesis that the MAP is generated locally through pressure depolarization of a circumscript volume of cells that (1) has sharp voltage gradients toward normal cells, (2) provides a strong local current source, and (3) when simulated with a circuit model creates the field potential recorded by the contact MAP electrode.

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