Can Peer Assessment Impact Self-efficacy During Small-Group Learning?

INTRODUCTION: While studies report positive correlations between students' perceptions of the learning environment and their reported self-efficacy, the role of peer assessment is poorly understood in this context. This study examines the process and impact of peer assessment on self-efficacy and perceptions of the learning environment during a small-group discussion-based course required of first-year medical students. METHODS: After spending time in small-group learning, students completed three peer assessments and reviewed three assessments of themselves. Analysis of the peer assessments included thematic coding of comments and word counts. Prior to and following the assessment period, students completed a survey including the Generalized Self-efficacy (GSE) Scale, and six locally-developed questions regarding the learning environment and perceptions of peer assessment. We performed paired-sample t tests to determine whether there were differences between the pre- and post-peer assessment surveys. The SUNY Upstate Institutional Review Board reviewed the study and determined it to be exempt. RESULTS: Peer assessment narratives referred most commonly to students' participation style and the need for greater participation. Word counts ranged widely. A paired sample t test indicated that the difference between pre and post peer assessment GSE scores was significant (P=.009), but the effect size was small (d=0.32). Perceptions of the learning environment did not change after the peer assessments. CONCLUSION: Peer assessment offers a potential strategy for enhancing self-efficacy in medical school small-group learning environments and requires few resources to implement, relative to the potential benefits.

Elevated zinc transporter ZnT3 in the dentate gyrus of mast cell-deficient mice.

Zinc is important in neurogenesis, but excessive levels can cause apoptosis and other pathologies leading to cognitive impairments. Mast cells are present in many brain regions including the hippocampus, an area rich in vesicular zinc. Mast cells contain zinc-rich granules and a well-developed mechanism for uptake of zinc ions; both features point to the potential for a role in zinc homeostasis. Prior work using the Timm stain supported this hypothesis, as increased labile zinc was detected in the hippocampus of mast cell-deficient mice compared to wild-type mice while no differences in total zinc were found between the two genotypes in the whole brain or other tissues. The current report further examines differences in zinc homeostasis between wild-type and mast cell-deficient mice by exploring the zinc transporter ZnT3, which transports labile zinc into synaptic vesicles. The first study used immunocytochemistry to localize ZnT3 within the mossy fibre layer of the hippocampus to determine whether there was differential expression of ZnT3 in wild-type versus mast cell-deficient mice. The second study used inductively coupled plasma mass spectrometry (ICP-MS) to determine total zinc content in the whole dentate gyrus of the two genotypes. The immunocytochemical results indicate that there are higher levels of ZnT3 localized to the mossy fibre layer of the dentate gyrus of mast cell-deficient mice than in wild-type mice. The ICP-MS data reveal no differences in total zinc in dentate gyrus as a whole. The results are consistent with the hypothesis that mast cells participate in zinc homeostasis at the level of synaptic vesicles.

Function of Metallothionein-3 in Neuronal Cells: Do Metal Ions Alter Expression Levels of MT3?

A study of factors proposed to affect metallothionein-3 (MT3) function was carried out to elucidate the opaque role MT3 plays in human metalloneurochemistry. Gene expression of Mt2 and Mt3 was examined in tissues extracted from the dentate gyrus of mouse brains and in human neuronal cell cultures. The whole-genome gene expression analysis identified significant variations in the mRNA levels of genes associated with zinc homeostasis, including Mt2 and Mt3. Mt3 was found to be the most differentially expressed gene in the identified groups, pointing to the existence of a factor, not yet identified, that differentially controls Mt3 expression. To examine the expression of the human metallothioneins in neurons, mRNA levels of MT3 and MT2 were compared in BE(2)C and SH-SY5Y cell cultures treated with lead, zinc, cobalt, and lithium. MT2 was highly upregulated by Zn2+ in both cell cultures, while MT3 was not affected, and no other metal had an effect on either MT2 or MT3.

Evidence for mast cell-mediated zinc homeostasis: Increased labile zinc in the hippocampus of mast-cell deficient mice.

The dentate gyrus of the hippocampus is a site of adult neurogenesis, and is also known to contain one of the highest concentrations of labile brain zinc (Zn), thought to aid in learning and memory by supporting neurogenesis. At the same time, it is known that unbound Zn, when present at excessive levels, decreases the formation of new neurons. Since mast cells contain Zn transporters capable of moving this essential element across their plasma membrane, as well as Zn-rich granules that are dispelled upon secretion, we reasoned that mast cells contribute to Zn homeostasis in this area of the brain, as they are found in greatest numbers in and around the dentate gyrus. This line of evidence was tested by comparing Timm-stained hippocampal sections of mast cell-deficient C57BL/6-KitW-sh/W-sh (Sash-/-) mice to those of mast cell-containing wild type (Sash+/+) animals. Mast cell deficient mice were found to have significantly increased Timm-positive staining as compared to controls, reflecting an increase in labile or bioactive Zn in this region. As we observed no change in total brain Zn (protein-bound plus unbound Zn), these increases indicate that mast cells may serve to bind what would otherwise be excessive or deleterious levels of labile Zn, or that they are able to recruit metallothionein proteins. Because elevated levels of labile Zn are observed in the brains of patients with neurodegenerative diseases such as Alzheimer's, the potential contribution of mast cells to these diseases remains a compelling one. Overall, these data support a role for mast cells in either establishing or maintaining Zn homeostasis in the brain in the service of health, while Zn dysregulation has the potential to reduce learning, memory, and ultimately organismal survival.