Student exam performance in flipped classroom sections is similar to that in active learning sections,and satisfaction with the flipped classroom hinges on attitudes toward learning from videos

ABSTRACT

The flipped classroom is a teaching innovation in which instructional content is delivered out of the classroom, often via videos, and the class period is used for application of the course material. While the popularity of the flipped classroom is growing exponentially, its benefits have not been extensively studied. In this study we compared three semesters of an undergraduate Genetics course that was non-flipped, but included a significant amount of active learning, to three semesters of a flipped course with the same content. Student exam performance was not statistically different between the active non-flipped and the flipped courses, suggesting that the benefits of the flipped environment may be similar to those achieved via active learning. We also examined student attitudes toward the flipped classroom, and found 56% of students were satisfied, 39% were dissatisfied, and 5% were neutral toward the flipped classroom. Our survey revealed that the clearest defining characteristic of dissatisfied students was not a dislike of classroom active learning activities. Rather, dissatisfied students disproportionately disliked, and had difficulty learning the course material, from videos.     

Reovirus guanylyltransferase is L2 gene product lambda 2.

Reovirus guanylyltransferase, studied as a covalent enzyme-GMP intermediate, was used to guanylate appropriate acceptor molecules in vitro to produce authentic cap structures. Guanylyltransferase activity was associated with lambda 2, the 140-kilodalton product of the L2 gene segment of reovirus serotypes 1 and 3.     

Mg++-sensitivity of neuromuscular transmission in two crustaceans: Correlation with blood Mg++ levels

Neuromuscular transmission was measured in muscles of spider crabs (Hyasareneus) and lobsters (Homarus americanus). Solutions containing 40 and 10 mM/1 Mg⁺⁺, which were approximately the same as those measured in the blood of Hyas and Homarus, respectively, were used to soak the preparations prior to testing. In Homarus, neuromuscular transmission was severely depressed by 40 mM Mg⁺⁺. In spider crabs, neuromuscular transmission was not severely depressed. Although the amount of transmitter released by nerve impulses was reduced, total membrane depolarization during trains of impulses was not reduced because a compensating increase in muscle fiber membrane resistance occurred in Hyas preparations exposed to 40 mM Mg⁺⁺. Hyas, but not Homarus, is physiologically adapted to function at relatively high blood Mg⁺⁺ concentrations.     

Antiapoptotic Bcl-2 family proteins BCL-xL and MCL-1 integrate neural progenitor survival and proliferation during postnatal cerebellar neurogenesis

The tendency of brain cells to undergo apoptosis in response to exogenous events varies across neural development, with apoptotic threshold dependent on proliferation state. Proliferative neural progenitors show a low threshold for apoptosis, while terminally differentiated neurons are relatively refractory. To define the mechanisms linking proliferation and apoptotic threshold, we examined the effect of conditionally deleting Bcl2l1, the gene that codes the antiapoptotic protein BCL-xL, in cerebellar granule neuron progenitors (CGNPs), and of co-deleting Bcl2l1 homologs, antiapoptotic Mcl-1, or pro-apoptotic Bax. We found that cerebella in conditional Bcl2l1-deleted (Bcl-xL^cKO) mice were severely hypoplastic due to the increased apoptosis of CGNPs and their differentiated progeny, the cerebellar granule neurons (CGNs). Apoptosis was highest as Bcl-xL^cKO CGNPs exited the cell cycle to initiate differentiation, with proliferating Bcl-xL^cKO CGNPs relatively less affected. Despite the overall reduction in cerebellar growth, SHH-dependent proliferation was prolonged in Bcl-xL^cKO mice, as more CGNPs remained proliferative in the second postnatal week. Co-deletion of Bax rescued the Bcl-xL^cKO phenotype, while co-deletion of Mcl-1 enhanced the phenotype. These findings show that CGNPs require BCL-xL to regulate BAX-dependent apoptosis, and that this role can be partially compensated by MCL-1. Our data further show that BCL-xL expression regulates MCL-1 abundance in CGNPs, and suggest that excessive MCL-1 in Bcl-xL^cKO mice prolongs CGNP proliferation by binding SUFU, resulting in increased SHH pathway activation. Accordingly, we propose that BCL-xL and MCL-1 interact with each other and with developmental mechanisms that regulate proliferation, to adjust the apoptotic threshold as CGNPs progress through postnatal neurogenesis to CGNs.Subject terms: Cell biology, Neuroscience