Recognizing Reflection: Computer-Assisted Analysis of First Year Medical Students' Reflective Writing.

BACKGROUND: Reflective writing is used throughout medical education to help students navigate their transformation into medical professionals. Assessment of reflective writing, however, is challenging; each available methodology of assessment has distinct advantages and disadvantages. We tested if combining two independent assessment mechanisms-a faculty-designed rubric and Academic Writing Analytics (AWA), an automated technique-could be used together to form a more robust form of evaluation. METHODS: We obtained reflective essays written by first year medical students as part of a clinical skills course. Faculty scored essays using a rubric designed to evaluate Integration, Depth, and Writing. The same essays were subjected to AWA analysis, which counted the number of reflective phrases indicative of Context, Challenge, or Change. RESULTS: Faculty scored the essays uniformly high, indicating that most students met the standard for reflection as described by the rubric. AWA identified over 1400 instances of reflective behavior within the essays, and there was significant variability in how often different types of reflective phrases were used by individual students. CONCLUSIONS: While data from faculty assessment or AWA alone is sufficient to evaluate reflective essays, combining these methods offer a richer and more valuable understanding of the student's reflection.

Hedgehog signaling and Tre1 regulate actin dynamics through PI(4,5)P2 to direct migration of Drosophila embryonic germ cells.

The Tre1 G-protein coupled receptor (GPCR) was discovered to be required for Drosophila germ cell (GC) coalescence almost two decades ago, yet the molecular events both upstream and downstream of Tre1 activation remain poorly understood. To gain insight into these events, we describe a bona fide null allele and both untagged and tagged versions of Tre1. We find that the primary defect with complete Tre1 loss is the failure of GCs to properly navigate, with GC mis-migration occurring from early stages. We find that Tre1 localizes with F-actin at the migration front, along with PI(4,5)P2; dPIP5K, an enzyme that generates PI(4,5)P2; and dWIP, a protein that binds activated Wiskott-Aldrich syndrome protein (WASP), which stimulates F-actin polymerization. We show that Tre1 is required for polarized accumulation of F-actin, PI(4,5)P2, and dPIP5K. Smoothened also localizes with F-actin at the migration front, and Hh, through Smo, increases levels of Tre1 at the plasma membrane and Tre1's association with dPIP5K.

Drosophila FoxL1 non-autonomously coordinates organ placement during embryonic development.

Determining how organs attain precise positioning within an organism is a crucial facet of developmental biology. The Fox family winged-helix transcription factors are known to play key roles in development of multiple organs. Drosophila FoxL1 (aka Fd64A) is dynamically expressed in embryos but its function is completely uncharacterized. FoxL1 is expressed in a single group of body wall - muscles in the 2nd and 3rd thoracic segments, in homologous abdominal muscles at earlier stages, and in the hindgut mesoderm from early through late embryogenesis. We show that FoxL1 expression in T2 and T3 is in VIS5, which is not a single muscle spanning the entire thorax, as previously published, but is, instead, three individual muscles, each spanning a single thoracic segment. We generate mutations in foxL1 and show that, surprisingly, none of the tissues that express FoxL1 are affected by its loss. Instead, loss of foxL1 results in defects in salivary gland positioning and morphology, as well as defects in the migration of hemocytes, germ cells and Malpighian tubules. We also show that FoxL1-dependent expression of secreted Sema2a in T3 VIS5 is required for normal salivary gland positioning. Altogether, these findings suggest that Drosophila FoxL1 functions like its mammalian counterpart in non-autonomously orchestrating the behaviors of surrounding tissues.

Outside-in signaling--a brief review of GPCR signaling with a focus on the Drosophila GPCR family.

G-protein-coupled receptors (GPCRs) are the largest family of receptors in many organisms, including worms, mice and humans. GPCRs are seven-transmembrane pass proteins that are activated by binding a stimulus (or ligand) in the extracellular space and then transduce that information to the inside of the cell through conformational changes. The conformational changes activate heterotrimeric G-proteins, which execute the downstream signaling pathways through the recruitment and activation of cellular enzymes. The highly specific ligand-GPCR interaction prompts an efficient cellular response, which is vital for the health of the cell and organism. In this Commentary, we review general features of GPCR signaling and then focus on the Drosophila GPCRs, which are not as well-characterized as their worm and mammalian counterparts. We discuss findings that the Drosophila odorant and gustatory receptors are not bona fide GPCRs as is the case for their mammalian counterparts. We also present here a phylogenetic analysis of the bona fide Drosophila GPCRs that suggest potential roles for several family members. Finally, we discuss recently discovered roles of GPCRs in Drosophila embryogenesis, a field we expect will uncover many previously unappreciated functions for GPCRs.

Building and specializing epithelial tubular organs: the Drosophila salivary gland as a model system for revealing how epithelial organs are specified, form and specialize.

The past two decades have witnessed incredible progress toward understanding the genetic and cellular mechanisms of organogenesis. Among the organs that have provided key insight into how patterning information is integrated to specify and build functional body parts is the Drosophila salivary gland, a relatively simple epithelial organ specialized for the synthesis and secretion of high levels of protein. Here, we discuss what the past couple of decades of research have revealed about organ specification, development, specialization, and death, and what general principles emerge from these studies.

The CrebA/Creb3-like transcription factors are major and direct regulators of secretory capacity.

Secretion occurs in all cells, with relatively low levels in most cells and extremely high levels in specialized secretory cells, such as those of the pancreas, salivary, and mammary glands. How secretory capacity is selectively up-regulated in specialized secretory cells is unknown. Here, we find that the CrebA/Creb3-like family of bZip transcription factors functions to up-regulate expression of both the general protein machinery required in all cells for secretion and of cell type-specific secreted proteins. Drosophila CrebA directly binds the enhancers of secretory pathway genes and is both necessary and sufficient to activate expression of every secretory pathway component gene examined thus far. Microarray profiling reveals that CrebA also up-regulates expression of genes encoding cell type-specific secreted components. Finally, we found that the human CrebA orthologues, Creb3L1 and Creb3L2, have the ability to up-regulate the secretory pathway in nonsecretory cell types.