Publications by authors named "Kristen Frenzel"

In this paper we share the first five of what we hope will be many profiles of neuroscientists from historically underrepresented or marginalized groups. This initial collection of profiles, meant to stake out the general territory for future offerings, takes as its subjects a fairly broad range of individuals from Nobel laureates to early career scientists and educators. The goal of this project is to facilitate the dissemination of materials neuroscience educators can use to highlight the scientific contributions and personal stories of scientists from historically marginalized groups, and has been developed more extensively in the Editorial that accompanies this collection (Frenzel and Harrington, 2021).

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Institutions of higher education are meant to provide opportunities for the growth and development of their students. As student bodies have become more diverse it would seem to follow that institutional efforts to satisfy this obligation would likewise need to change. Despite increases in the numbers of historically underrepresented students entering higher education, the proportion of these students who graduate continues to lag behind that of students who are not historically underrepresented.

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Epilepsy and seizure generation are at the center of this case study narrative. By exploring the nature of genetic mutations in voltage-gated sodium channels students will solidify fundamental concepts involving action potential generation and roles for excitatory and inhibitory neurons in the central nervous system. Students will wrestle with primary data, developing analytical and quantitative skills, and generate evidence-based hypotheses and predictions.

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For the past six years, we have been teaching a neuroscience for non-science majors course titled "From Botox to Behavior: Neuroscience for non-scientists." The primary objectives for this course are to create science literate students using neuroscience concepts as the foundation. The evidence from our course assessments suggest that the students are learning fundamental concepts and developing skills of source evalution, using evidence in an argument and appreciating the role of neuroscience in society.

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Students work through this Problem-Based Learning Case in order to discover how Nora ended up blue lipped and non-responsive. By exploring fundamental mechanisms of neuronal communication, students examine facts, research concepts, and propose hypotheses about how Nora's physiology was disrupted to cause her respiratory distress. The dramatic context supports student learning at many levels - from systems neurophysiology to synaptic pharmacology.

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Jak2 is a member of the Janus family of tyrosine kinases and is involved in cytokine signaling. As a part of a study to determine biological functions of Jak2, we used molecular modeling to identify W1038 as a residue that is critical for tyrosine kinase function. Mutation of W1038, in tandem with E1046, generates a dominant-negative form of the Jak2 protein.

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The resin angiotensin system (RAS) plays an essential role in blood pressure regulation and electrolyte homeostasis. The effecter peptide of the RAS, angiotensin II, is produced by angiotensin converting enzyme (ACE) in multiple tissues. Genetic deletion of ACE in mice resulted a phenotype of low blood pressure, anemia and kidney defects.

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The renin angiotensin system (RAS) is a central player in blood pressure control. Its effector peptide, angiotensin II, regulates blood pressure through coordinated actions in multiple tissues. The RAS is generally considered to be an endocrine system, and angiotensin II to be a circulating hormone.

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Despite several decades of research into the renin-angiotensin system, new aspects of this endocrine system are elucidated every few years, expanding its role not only in hypertension but also in diabetes, oncology, and cardiology. In this review, we describe newly recognized physiologic actions of the angiotensin-converting enzyme (ACE). These include the role of local versus systemic ACE in maintaining blood pressure, the physiology of bradykinin accumulation during ACE inactivation, and the role of alternate "non-angiotensin" substrates and potential non-enzymatic properties of ACE.

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Angiotensin-converting enzyme (ACE) produces the vasoconstrictor angiotensin II. The ACE protein is composed of two homologous domains, each binding zinc and each independently catalytic. To assess the physiologic significance of the two ACE catalytic domains, we used gene targeting in mice to introduce two point mutations (H395K and H399K) that selectively inactivated the ACE N-terminal catalytic site.

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