The implementation of clay modeling and rat dissection into the human anatomy and physiology curriculum of a large urban community college.

After a considerable amount of research and experimentation, cat dissection was replaced with rat dissection and clay modeling in the human anatomy and physiology laboratory curricula at La Guardia Community College (LAGCC), a large urban community college of the City University of New York (CUNY). This article describes the challenges faculty overcame and the techniques used to solve them. Methods involved were: developing a laboratory manual in conjunction with the publisher, holding training sessions for faculty and staff, the development of instructional outlines for students and lesson plans for faculty, the installation of storage facilities to hold mannequins instead of cat specimens, and designing mannequin clean-up techniques that could be used by more than one thousand students each semester. The effectiveness of these curricular changes was assessed by examining student muscle practical examination grades and the responses of faculty and students to questionnaires. The results demonstrated that the majority of faculty felt prepared to teach using clay modeling and believed the activity was effective in presenting lesson content. Students undertaking clay modeling had significantly higher muscle practical examination grades than students undertaking cat dissection, and the majority of students believed that clay modeling was an effective technique to learn human skeletal, respiratory, and cardiovascular anatomy, which included the names and locations of blood vessels. Furthermore, the majority of students felt that rat dissection helped them learn nervous, digestive, urinary, and reproductive system anatomy. Faculty experience at LAGCC may serve as a resource to other academic institutions developing new curricula for large, on-going courses.

Clay modeling as a method to learn human muscles: A community college study.

The efficacy of clay modeling compared with cat dissection for human muscle identification was examined over two semesters at LaGuardia Community College in Queens, NY. The 181 students in 10 sections in this study were randomly distributed into control (cat dissection) and experimental (clay modeling) groups, and the results of the muscle practical examination were analyzed. The clay-modeling group was significantly better at identifying human muscles on human models than the cat-dissection group, and was as good at identifying muscles on their self-made clay mannequins as the cat-dissection group was at identifying cat muscle on their specimens. This study demonstrated that clay modeling is more effective than cat dissection for learning human muscles at the community college level.

Expression of human ERG K+ channels in the mouse heart exerts anti-arrhythmic activity.

OBJECTIVE: The K(+) channel encoded by the human ether-a-go-go-related gene (HERG) is crucial for repolarization in the human heart. In order to investigate the impact of HERG current (I(Kr)) on the incidence of cardiac arrhythmias, we generated a transgenic mouse expressing HERG specifically in the heart. METHODS AND RESULTS: ECG recordings at baseline showed no obvious difference between transgenic and wild-type (WT) mice with the exception of the T wave, which was more negative in transgenic mice than in WT mice. E4031 (20 mg/kg) prolonged the QTc interval and flattened the T wave in transgenic mice, but not in WT mice. Injection of BaCl(2) (25 mg/kg) induced short runs of ventricular tachycardia in 9/10 WT mice, but not in transgenic animals. Atrial pacing reproducibly induced atrial tachyarrhythmias in 11/15 WT mice. In contrast, atrial arrhythmia was inducible in only 2/11 transgenic mice. When pretreated with dofetilide (10 mg/kg), transgenic mice were as sensitive to experimental arrhythmias as WT mice. Microelectrode studies showed that atrial action potentials have a steeper slope of duration-rate adaptation in WT than in transgenic mice. Transgenic mice were also characterized by a post-repolarization refractoriness, which could result from the substantial amount of I(Kr) subsisting after repolarization as assessed with action potential-clamp experiments and simulations with a model of the transgenic mouse action potential. CONCLUSION: HERG expression in the mouse heart can protect against experimental induction of arrhythmias. This is the first report of such a protective effect of HERG in vivo.

Regulatory actions of the A-kinase anchoring protein Yotiao on a heart potassium channel downstream of PKA phosphorylation.

A-kinase anchoring proteins (AKAPs) are thought to be passive members of protein complexes that coordinate the association of cAMP-dependent protein kinase A (PKA) with cellular substrates to facilitate targeted PKA protein phosphorylation. I(Ks), the slow heart potassium current, is carried by the I(Ks) potassium channel, a substrate for PKA phosphorylation in response to sympathetic nerve stimulation, is a macromolecular complex that includes the KCNQ1 alpha subunit, the KCNE1 regulatory subunit, and the AKAP Yotiao. Disruption of this regulation by mutation in the long QT syndrome is associated with elevated risk of sudden death. Here, we have studied the effects of the AKAP Yotiao on the function of the I(Ks) channel that had been mutated to simulate channel phosphorylation, and we report direct AKAP-mediated alteration of channel function distinct from its role in the coordination of channel phosphorylation by PKA. These data reveal previously undescribed actions of Yotiao that occur subsequent to channel phosphorylation and provide evidence that this adaptor protein also may serve as an effector in regulating this important ion channel.

The Na+ channel inactivation gate is a molecular complex: a novel role of the COOH-terminal domain.

Electrical activity in nerve, skeletal muscle, and heart requires finely tuned activity of voltage-gated Na+ channels that open and then enter a nonconducting inactivated state upon depolarization. Inactivation occurs when the gate, the cytoplasmic loop linking domains III and IV of the alpha subunit, occludes the open pore. Subtle destabilization of inactivation by mutation is causally associated with diverse human disease. Here we show for the first time that the inactivation gate is a molecular complex consisting of the III-IV loop and the COOH terminus (C-T), which is necessary to stabilize the closed gate and minimize channel reopening. When this interaction is disrupted by mutation, inactivation is destabilized allowing a small, but important, fraction of channels to reopen, conduct inward current, and delay cellular repolarization. Thus, our results demonstrate for the first time that physiologically crucial stabilization of inactivation of the Na+ channel requires complex interactions of intracellular structures and indicate a novel structural role of the C-T domain in this process.