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This paper describes two pilot studies investigating the use of concept mapping for assessing students' conceptual knowledge at a given point and over time. In Study 1, three groups constructed concept maps in response to the question, "What are the 10-20 most important concepts in biomedical engineering and how are they related?" Group differences were consistent with expert-novice distinctions in structural knowledge: faculty generated dense networks of higher-order principles and their applications while students generated fewer connections among concepts pertaining largely to domain content. Study 2 assessed students' conceptual understanding of the biomedical engineering design process in a yearlong design course at three different time points. Later maps contained a greater number of concepts, more precise vocabulary, and were more valid. These findings are discussed in terms of their implications for theories about the structure of knowledge and identification of the skills associated with a culture of practice. I. INTRODUCTIONBioengineering (BE) courses typically adopt traditional approaches to student assessment such as asking students to answer fact-based questions and derive correct solutions. While valuable for tapping forms of knowledge labeled by cognitive psychologists as declarative (i.e., knowing what) and procedural (i.e., knowing how) [1], these forms of assessment often fail to tap a third and vital asset in problem-solving, conditional knowledge (i.e., knowing why and when). Addressing gaps between traditional forms of problem-solving and assessment in the classroom and the day-today demands of the workplace, the Vanderbilt-NorthwesternTexas-Harvard/MIT Engineering Research Center (VaNTH ERC) is investigating alternative and more comprehensive methods for capturing and assessing what students know, and developing tools that help students integrate an array of diverse competencies across the BE curriculum. One potentially useful tool for achieving these goals is concept mapping.Invented during the 1970s by Novak and his colleagues at Cornell University, a concept map looks like a flow chart. However, instead of "mapping the linear or logical structure of knowledge, concept maps reflect the psychological structure of knowledge [2]." Theoretically, knowledge functions as a semantic network [3]. Thus, learning is not only the acquisition and understanding of concepts but also the construction of meaningful links among concepts [4]. Consistent with these theoretical perspectives, concept maps are composed of interrelated elements: nodes, directed lines and labels. Nodes represent concepts. Concepts are defined as "perceived regularities in events or objects, or records of events or objects, designated by a label [5]." For example, "engineering" and "experimentation" are concepts. Lines represent relations among concepts. Labels in the lines describe the nature of those relations (e.g., "leads to") while arrowheads indicate the direction of the relationship. The combination of a pair of con...

Abstract-Although atrial fibrillation is the most common serious cardiac arrhythmia, the fundamental molecular pathways remain undefined. Mutations in KCNQ1, one component of a sympathetically activated cardiac potassium channel complex, cause familial atrial fibrillation, although the mechanisms in vivo are unknown. We show here that mice with deletion of the KCNQ1 protein partner KCNE1 have spontaneous episodes of atrial fibrillation despite normal atrial size and structure. Isoproterenol abolishes these abnormalities, but vagomimetic interventions have no effect. Whereas loss of KCNE1 function prolongs ventricular action potentials in humans, KCNE1 Ϫ/Ϫ mice displayed unexpectedly shortened atrial action potentials, and multiple potential mechanisms were identified: (1) K ϩ currents (total and those sensitive to the KCNQ1 blocker chromanol 293B) were significantly increased in atrial cells from KCNE1 Ϫ/Ϫ mice compared with controls, and (2) when CHO cells expressing KCNQ1 and KCNE1 were pulsed very rapidly (at rates comparable to the normal mouse heart and to human atrial fibrillation), the sigmoidicity of I Ks activation prevented current accumulation, whereas cells expressing KCNQ1 alone displayed marked current accumulation at these very rapid rates. Thus, KCNE1 deletion in mice unexpectedly leads to increased outward current in atrial myocytes, shortens atrial action potentials, and enhances susceptibility to atrial fibrillation. Key Words: arrhythmia Ⅲ atrial fibrillation Ⅲ cardiac electrophysiology Ⅲ mouse Ⅲ potassium channels A trial fibrillation (AF) is a major public health problem, affecting 2% of people over the age of 60 and 9% of people over 80. 1 AF is the proximate cause of 20% to 25% of strokes and is implicated in disability attributable to heart failure. 2 Despite the magnitude of this problem, the development of increasingly sophisticated animal models, and advances in pharmacological and nonpharmacological therapy, our understanding of the molecular effector mechanisms underlying AF remains incomplete. 3 Whereas the critical mass hypothesis suggested that the mouse atrium was too small to support AF, 4,5 spontaneous atrial arrhythmias are now well-documented in mice with atrial dilation. 6 -9 However, atrial dilation results in multiple changes in gene expression that complicate identification and validation of AF effector molecules. A strong familial component in AF 10 -12 suggests that identification of predisposing DNA variants may provide new insights into underlying biology. Indeed, rare kindreds with a high incidence of AF have been described, and 3 disease genes, each linked to arrhythmias in a single kindred, 13-15 as well as 3 other loci, 16 -18 have been reported. Mutations in one of these disease genes, KCNQ1, also cause the most common form of the congenital long QT syndrome. 19 KCNQ1 associates with the ancillary subunit KCNE1 to generate the adrenergically regulated 20 potassium current I Ks . Mutations in either gene reduce I Ks prolong action potentials in human ventricle ...

The minimal lethal concentration of ozone in water was determined for three bacterial species: Escherichia coli, Bacillus cereus , and Bacillus megaterium . A contact period of 5 min was selected. The lethal threshold concentration for the cells of B. cereus was 0.12 mg/liter while that for E. coli and B. megaterium was 0.19 mg/liter. Low concentrations of ozone were ineffective when organic matter was present to interfere with the action of ozone on the bacterial cells. Also determined during the study was the sensitivity of spores of B. cereus and B. megaterium to ozone in water. The threshold concentration required to kill the spores of both species was 2.29 mg/liter. The cells and spores of these organisms exhibited the “all-or-none” die-away phenomenon normally associated with ozone treatment.