Collaborative Testing in Medical Education: Student Perceptions and Long-Term Knowledge Retention.

Collaborative testing blends collaborative learning and assessment, engaging small groups of students in answering exam questions as a team. Previous studies have shown that collaborative testing promotes increased student performance and short-term knowledge retention over individual testing alone. In this mixed-methods study, we examined the effects of collaborative testing on preclinical medical students' long-term retention of basic science knowledge, as well as students' approaches and perceptions of collaborative testing.

Learning by doing: construction and manipulation of a skeletal muscle model during lecture.

Active learning, "learning by doing," enhances student performance on examinations and improves student retention of course content. Active learning also provides inquiry-based, collaborative, and problem-solving activities that promote curiosity, skepticism, objectivity, and the use of scientific reasoning. To incorporate active learning into our undergraduate anatomy and physiology course of 70 nursing students, students constructed working physical models of skeletal muscle during the scheduled class time.

Parvalbumin isoforms differentially accelerate cardiac myocyte relaxation kinetics in an animal model of diastolic dysfunction.

The cytosolic Ca(2+)/Mg(2+)-binding protein alpha-parvalbumin (alpha-Parv) has been shown to accelerate cardiac relaxation; however, beyond an optimal concentration range, alpha-Parv can also diminish contractility. Mathematical modeling suggests that increasing Parv's Mg(2+) affinity may lower the effective concentration of Parv ([Parv]) to speed relaxation and, thus, limit Parv-mediated depressed contraction. Naturally occurring alpha/beta-Parv isoforms show divergence in amino acid primary structure (57% homology) and cation-binding affinities, with beta-Parv having an estimated 16% greater Mg(2+) affinity and approximately 200% greater Ca(2+) affinity than alpha-Parv.

Spinal cord injury alters cardiac electrophysiology and increases the susceptibility to ventricular arrhythmias.

The autonomic nervous system modulates cardiac electrophysiology and abnormalities of autonomic function are known to increase the risk of ventricular arrhythmias. The abnormal and unstable autonomic control of the cardiovascular system following spinal cord injury also is well known. For example, individuals with mid-thoracic spinal cord injury have elevated resting heart rates, increased blood pressure variability, episodic bouts of life-threatening hypertension as part of a condition termed autonomic dysreflexia, and elevated sympathetic activity above the level of the lesion.

Student retention of course content is improved by collaborative-group testing.

We recently reported that collaborative testing (i.e., group test taking) increased student performance on quizzes.

Increased susceptibility to ventricular arrhythmias is associated with changes in Ca2+ regulatory proteins in paraplegic rats.

Paraplegia may increase susceptibility to ventricular arrhythmias by altering the autonomic control of the heart. Altered cardiac autonomic control has been documented to change the expression of genes that encode cardiac Ca2+ regulatory proteins. Therefore, we tested the hypothesis that paraplegia alters cardiac electrophysiology with concomitant changes in Ca2+ regulatory proteins in a manner that increases the susceptibility to ventricular arrhythmias.

Paraplegia differentially increases arterial blood pressure related cardiovascular disease risk factors in normotensive and hypertensive rats.

Older individuals (>50 years of age) are increasingly sustaining spinal cord injuries (SCI) and often have pre-existing medical conditions, including hypertension. Furthermore, the life expectancy of individuals with paraplegia has increased to near that of able-bodied individuals. Thus, chronic diseases associated with aging (e.

Daily exercise normalizes the number of diaphorase (NOS) positive neurons in the hypothalamus of hypertensive rats.

It is well known that nitric oxide (NO), within the paraventricular nucleus (PVN) of the hypothalamus, mediates sympatho-inhibition via an inhibitory GABA-ergic mechanism. Furthermore, the inhibitory GABA-ergic mechanism is impaired in the spontaneously hypertensive rat (SHR). These data suggest that the NO system, within the PVN, may also be impaired in the SHR.