Individual variation in undergraduate student metacognitive monitoring and error detection during biology model evaluation

IntroductionModels are a primary mode of science communication and preparing university students to evaluate models will allow students to better construct models and predict phenomena. Model evaluation relies on students’ subject-specific knowledge, perception of model characteristics, and confidence in their knowledge structures.MethodsFifty first-year college biology students evaluated models of concepts from varying biology subject areas with and without intentionally introduced errors. Students responded with ‘error’ or ‘no error’ and ‘confident’ or ‘not confident’ in their response.ResultsOverall, students accurately evaluated 65% of models and were confident in 67% of their responses. Students were more likely to respond accurately when models were drawn or schematic (as opposed to a box-and-arrow format), when models had no intentional errors, and when they expressed confidence. Subject area did not affect the accuracy of responses.DiscussionVariation in response patterns to specific models reflects variation in model evaluation abilities and suggests ways that pedagogy can support student metacognitive monitoring during model-based reasoning. Error detection is a necessary step towards modeling competence that will facilitate student evaluation of scientific models and support their transition from novice to expert scientists

A Community-Building Framework for Collaborative Research Coordination across the Education and Biology Research Disciplines

Since 2009, the U.S. National Science Foundation Directorate for Biological Sciences has funded Research Coordination Networks (RCN) aimed at collaborative efforts to improve participation, learning, and assessment in undergraduate biology education (UBE). RCN-UBE projects focus on coordination and communication among scientists and educators who are fostering improved and innovative approaches to biology education. When faculty members collaborate with the overarching goal of advancing undergraduate biology education, there is a need to optimize collaboration between participants in order to deeply integrate the knowledge across disciplinary boundaries. In this essay we propose a novel guiding framework for bringing colleagues together to advance knowledge and its integration across disciplines, the “Five ‘C’s’ of Collaboration: Commitment, Collegiality, Communication, Consensus, and Continuity.” This guiding framework for professional network practice is informed by both relevant literature and empirical evidence from community-building experience within the RCN-UBE Advancing Competencies in Experimentation–Biology (ACE-Bio) Network. The framework is presented with practical examples to illustrate how it might be used to enhance collaboration between new and existing participants in the ACE-Bio Network as well as within other interdisciplinary networks

The Basic Competencies of Biological Experimentation: Concept-Skill Statements

This biological experimentation competencies map is a model created by members of the ACE-Bio Network of seven areas a competent biologist calls in when doing experimentation in biology. Each competency is represented by a summary word on a uniquely colored segment of the model. For presentation convenience, the seven major areas within experimentation in biology are mapped onto tables in a linear manner. However, this is not meant to convey a particular order that one must follow during experimentation. The areas are given equal weight and flexible order of their use throughout the process of experimentation. This work is meant to provide a framework for ACE Bio Network participants and other instructors or academic leaders in the biological sciences to study implementation of experimentation activities and assessments across diverse institutional and curricular contexts. In addition to the document in pdf format, another link provides the file in MSWord format so that users can easily modify it to guide assessment of student learning about experimentation, undergraduate biology instruction, curriculum development, professional faculty development, program evaluation, or review of research literature in a way that is appropriate to their own context

Common mouse models of tauopathy reflect early but not late human disease

BACKGROUND: Mouse models that overexpress human mutant Tau (P301S and P301L) are commonly used in preclinical studies of Alzheimer’s Disease (AD) and while several drugs showed therapeutic effects in these mice, they were ineffective in humans. This leads to the question to which extent the murine models reflect human Tau pathology on the molecular level. METHODS: We isolated insoluble, aggregated Tau species from two common AD mouse models during different stages of disease and characterized the modification landscape of the aggregated Tau using targeted and untargeted mass spectrometry-based proteomics. The results were compared to human AD and to human patients that suffered from early onset dementia and that carry the P301L Tau mutation. RESULTS: Both mouse models accumulate insoluble Tau species during disease. The Tau aggregation is driven by progressive phosphorylation within the proline rich domain and the C-terminus of the protein. This is reflective of early disease stages of human AD and of the pathology of dementia patients carrying the P301L Tau mutation. However, Tau ubiquitination and acetylation, which are important to late-stage human AD are not represented in the mouse models. CONCLUSION: AD mouse models that overexpress human Tau using risk mutations are a suitable tool for testing drug candidates that aim to intervene in the early formation of insoluble Tau species promoted by increased phosphorylation of Tau. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13024-023-00601-y

An image analysis toolbox for high-throughput C. elegans assays

We present a toolbox for high-throughput screening of image-based Caenorhabditis elegans phenotypes. The image analysis algorithms measure morphological phenotypes in individual worms and are effective for a variety of assays and imaging systems. This WormToolbox is available through the open-source CellProfiler project and enables objective scoring of whole-worm high-throughput image-based assays of C. elegans for the study of diverse biological pathways that are relevant to human disease.National Institutes of Health (U.S.) (U54 EB005149

CAG repeat not polyglutamine length determines timing of Huntington’s disease onset

Variable, glutamine-encoding, CAA interruptions indicate that a property of the uninterrupted HTT CAG repeat sequence, distinct from the length of huntingtin’s polyglutamine segment, dictates the rate at which Huntington’s disease (HD) develops. The timing of onset shows no significant association with HTT cis-eQTLs but is influenced, sometimes in a sex-specific manner, by polymorphic variation at multiple DNA maintenance genes, suggesting that the special onset-determining property of the uninterrupted CAG repeat is a propensity for length instability that leads to its somatic expansion. Additional naturally occurring genetic modifier loci, defined by GWAS, may influence HD pathogenesis through other mechanisms. These findings have profound implications for the pathogenesis of HD and other repeat diseases and question the fundamental premise that polyglutamine length determines the rate of pathogenesis in the “polyglutamine disorders.

Genetic and functional analyses point to FAN1 as the source of multiple Huntington Disease modifier effects

A recent genome-wide association study of Huntington’s disease (HD) implicated genes involved in DNA maintenance processes as modifiers of onset, including multiple genome-wide significant signals in a chr15 region containing the DNA repair gene FAN1. Here, we have carried out detailed genetic, molecular and cellular investigation of the modifiers at this locus. We find that missense changes within or near the DNA binding domain (p.Arg507His and p.Arg377Trp) reduce FAN1's DNA binding activity and its capacity to rescue mitomycin C-induced cytotoxicity, accounting for two infrequent onset-hastening modifier signals. We also identified a third onset-hastening modifier signal whose mechanism of action remains uncertain but does not involve an amino acid change in FAN1. We present additional evidence that a frequent onset-delaying modifier signal does not alter FAN1 coding sequence but is associated with increased FAN1 mRNA expression in the cerebral cortex. Consistent with these findings and other cellular overexpression/suppression studies, knock out of FAN1 increased CAG repeat expansion in HD induced pluripotent stem cells. Together, these studies support the process of somatic CAG repeat expansion as a therapeutic target in HD, and clearly indicate that multiple genetic variations act by different means through FAN1 to influence HD onset in a manner that is largely additive, except in the rare circumstance that two onset-hastening alleles are present. Thus, an individual’s particular combination of FAN1 haplotypes may influence their suitability for HD clinical trials, particularly if the therapeutic agent aims to reduce CAG repeat instability

Modification of Huntington's disease by short tandem repeats

Expansions of glutamine-coding CAG trinucleotide repeats cause a number of neurodegenerative diseases, including Huntington's disease (HD) and several of the spinocerebellar ataxias (SCAs). In general, age-at-onset of the polyglutamine diseases is inversely correlated with the size of the respective inherited expanded CAG repeat. Expanded CAG repeats are also somatically unstable in certain tissues, and age-at-onset of HD corrected for individual HTT CAG repeat length (i.e., residual age-at-onset), is modified by repeat instability-related DNA maintenance/repair genes as demonstrated by recent genome-wide association studies (GWAS). Modification of one polyglutamine disease (e.g., HD) by the repeat length of another (e.g., ATXN3, CAG expansions in which cause SCA3) has also been hypothesized. Consequently, we determined whether age-at-onset in HD is modified by the CAG repeats of other polyglutamine disease genes. We found that the CAG measured repeat sizes of other polyglutamine disease genes were polymorphic in HD participants but did not influence HD age-at-onset. Additional analysis focusing specifically on ATXN3 in a larger sample set (n = 1,388) confirmed the lack of association between HD residual age-at-onset and ATXN3 CAG repeat length. Additionally, neither our HD onset modifier GWAS single nucleotide polymorphism (SNP) data nor imputed short tandem repeat (STR) data supported involvement of other polyglutamine disease genes in modifying HD. By contrast, our GWAS based on imputed STRs revealed significant modification signals for other genomic regions. Together, our STR GWAS show that modification of HD is associated with STRs that do not involve other polyglutamine disease-causing genes, refining the landscape of HD modification and highlighting the importance of rigorous data analysis, especially in genetic studies testing candidate modifiers

Tai Chi on psychological well-being: systematic review and meta-analysis

<p>Abstract</p> <p>Background</p> <p>Physical activity and exercise appear to improve psychological health. However, the quantitative effects of Tai Chi on psychological well-being have rarely been examined. We systematically reviewed the effects of Tai Chi on stress, anxiety, depression and mood disturbance in eastern and western populations.</p> <p>Methods</p> <p>Eight English and 3 Chinese databases were searched through March 2009. Randomized controlled trials, non-randomized controlled studies and observational studies reporting at least 1 psychological health outcome were examined. Data were extracted and verified by 2 reviewers. The randomized trials in each subcategory of health outcomes were meta-analyzed using a random-effects model. The quality of each study was assessed.</p> <p>Results</p> <p>Forty studies totaling 3817 subjects were identified. Approximately 29 psychological measurements were assessed. Twenty-one of 33 randomized and nonrandomized trials reported that 1 hour to 1 year of regular Tai Chi significantly increased psychological well-being including reduction of stress (effect size [ES], 0.66; 95% confidence interval [CI], 0.23 to 1.09), anxiety (ES, 0.66; 95% CI, 0.29 to 1.03), and depression (ES, 0.56; 95% CI, 0.31 to 0.80), and enhanced mood (ES, 0.45; 95% CI, 0.20 to 0.69) in community-dwelling healthy participants and in patients with chronic conditions. Seven observational studies with relatively large sample sizes reinforced the beneficial association between Tai Chi practice and psychological health.</p> <p>Conclusions</p> <p>Tai Chi appears to be associated with improvements in psychological well-being including reduced stress, anxiety, depression and mood disturbance, and increased self-esteem. Definitive conclusions were limited due to variation in designs, comparisons, heterogeneous outcomes and inadequate controls. High-quality, well-controlled, longer randomized trials are needed to better inform clinical decisions.</p