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My methodological choices for this study included the use of one-on-one, task-based clinical interviews which were video and audio recorded. Participants were chosen on the basis of selection criteria applied to a pool of volunteers from junior-level applied linear algebra classes. I conducted both generative and convergent analyses in terms of Clement’s (2000) continuum of research purposes. The generative analysis involved an exploration of the data (in transcript form). The convergent analysis involved the analysis of two student interviews through the lenses of Duval’s (1997, 2006, 2017) Theory of Semiotic Representation Registers and a theory I propose, the Theory of Quantitative Systems.
All participants concluded that for the four representations in this study, the notation was varying while the solution was invariant. Their descriptions of what was represented by the various representations fell into distinct categories. Further, the students employed visual techniques, heuristics, metaphors, and mathematical computation to account for translations between the various representations.
Theoretically, I lay out some constructs that may help with awareness of the complexity in linear algebra. While there are many rich concepts in linear algebra, challenges may stem from less-than-robust communication. Further, mathematics at the level of linear algebra requires a much broader perspective than that of the ordinary algebra of real numbers. Empirically, my results and findings provide important insights into students’ conceptions. The study revealed that students consider and/or can have their interest piqued by such things as changes in register.
The lens I propose along with the empirical findings should stimulate conversations that result in linear algebra courses most beneficial to students. This is especially important since students who encounter undue difficulties may alter their intended plans of study, plans which would lead them into careers in STEM (Science, Technology, Engineering, & Mathematics) fields.
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Background: Androgens bind to the androgen receptor (AR) in prostate cells and are essential survival factors for healthy prostate epithelium. Most untreated prostate cancers retain some dependence upon the AR and respond, at least transiently, to androgen ablation therapy. However, the relationship between endogenous androgen levels and cancer etiology is unclear. High levels of androgens have traditionally been viewed as driving abnormal proliferation leading to cancer, but it has also been suggested that low levels of androgen could induce selective pressure for abnormal cells. We formulate a mathematical model of androgen regulated prostate growth to study the effects of abnormal androgen levels on selection for pre-malignant phenotypes in early prostate cancer development.
Results: We find that cell turnover rate increases with decreasing androgen levels, which may increase the rate of mutation and malignant evolution. We model the evolution of a heterogeneous prostate cell population using a continuous state-transition model. Using this model we study selection for AR expression under different androgen levels and find that low androgen environments, caused either by low serum testosterone or by reduced 5α-reductase activity, select more strongly for elevated AR expression than do normal environments. High androgen actually slightly reduces selective pressure for AR upregulation. Moreover, our results suggest that an aberrant androgen environment may delay progression to a malignant phenotype, but result in a more dangerous cancer should one arise.
Conclusions: The model represents a useful initial framework for understanding the role of androgens in prostate cancer etiology, and it suggests that low androgen levels can increase selection for phenotypes resistant to hormonal therapy that may also be more aggressive. Moreover, clinical treatment with 5α-reductase inhibitors such as finasteride may increase the incidence of therapy resistant cancers.
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appears in a smaller region inside of the tumor. Simulations show that if the aggressive strain focuses its efforts on proliferating and does not contribute to angiogenesis signaling when in a hypoxic state, a hypertumor will form. More importantly, this resultant aggressive tumor is paradoxically prone to extinction and hypothesize is the cause of necrosis in many vascularized tumors.