Reflective Writing in Teacher Education in China: Insights from Systemic Functional Linguistics

This article aims to demonstrate the application of theory to teaching practice by examining how two teacher educators drew upon systemic functional linguistics (SFL) as a pedagogical and analytical tool to inform their teaching of reflective writing to Mandarin-dominant teacher candidates enrolled in an ESOL course within an educator preparation program at a university using English Medium Instruction (EMI) in China. First, the authors describe how they incorporated the SFL appraisal framework into their teaching to bring their multilingual student writers’ attention to the language of evaluation as they prepared to construct reflective language learning autobiographies. Second, the authors demonstrate how SFL-informed text analysis of the appraisal resources used within students’ written reflections deepened their understanding of their students’ reflective writing practices and informed their teaching and course development. The article concludes with suggestions for using the SFL appraisal framework to support the reflective writing of their multilingual teacher candidates

Creating a Linguistically-Responsive Intervention for Developing Readers: A Formative Experiment with a Teacher Study Group

University of Minnesota Ph.D. dissertation. May 2017. Major: Teaching and Learning. Advisor: Lori Helman. 1 computer file (PDF); viii, 192 pages.How are we to ensure that emergent bilinguals in early elementary settings receive linguistically-responsive reading interventions in response to intervention (RtI) frameworks? One way is to harness the collective expertise of classroom teachers, reading interventionists, and English language learner teachers. A collaborative relationship amongst these crucial school personnel is warranted in order to support the implementation of evidence-based practices in intervention, language development, and assessment. The goal of this study was to create, implement, and study a linguistically-responsive reading intervention for emergent bilinguals in an elementary RtI setting. Alongside a teacher study group that consisted of two classroom teachers, a reading interventionist, and an English language learner teacher, the teachers and I co-constructed and implemented the intervention. I used a formative experiment framework to conduct and execute the study. In six phases of design, I collected qualitative and quantitative data. Qualitative data collection included transcripts from teacher study group sessions, observations of teaching and learning in the intervention, interviews, and document review. Quantitative data collection included weekly reading assessment data and sentence repetition measures. Results indicate that language and reading development were fore fronted as a result of teachers’ collaborative efforts. Teachers who implemented the intervention contend that the strategies helped students’ overall comprehension. Students in the linguistically-responsive intervention showed growth in reading and language outcomes

Annotated Bibliography of Research in the Teaching of English

Since 2003, RTE has published the annual “Annotated Bibliography of Research in the Teaching of English,” and we are proud to share these curated and annotated citations once again. The goal of the annual bibliography is to offer a synthesis of the research published in the area of English language arts within the past year that may be of interest to RTE readers. Abstracted citations and those featured in the “Other Related Research” sections were published, either in print or online, between June 2019 and June 2020. The bibliography is divided into nine subject area sections. A three-person team of scholars with diverse research interests and background experiences in preK–16 educational settings reviewed and selected the manuscripts for each section using library databases and leading empirical journals. Each team abstracted significant contributions to the body of peer-reviewed studies that addressed the current research questions and concerns in their topic area

Inhibition of the Mitochondrial Enzyme ABAD Restores the Amyloid-β-Mediated Deregulation of Estradiol

Alzheimer's disease (AD) is a conformational disease that is characterized by amyloid-β (Aβ) deposition in the brain. Aβ exerts its toxicity in part by receptor-mediated interactions that cause down-stream protein misfolding and aggregation, as well as mitochondrial dysfunction. Recent reports indicate that Aβ may also interact directly with intracellular proteins such as the mitochondrial enzyme ABAD (Aβ binding alcohol dehydrogenase) in executing its toxic effects. Mitochondrial dysfunction occurs early in AD, and Aβ's toxicity is in part mediated by inhibition of ABAD as shown previously with an ABAD decoy peptide. Here, we employed AG18051, a novel small ABAD-specific compound inhibitor, to investigate the role of ABAD in Aβ toxicity. Using SH-SY5Y neuroblastoma cells, we found that AG18051 partially blocked the Aβ-ABAD interaction in a pull-down assay while it also prevented the Aβ42-induced down-regulation of ABAD activity, as measured by levels of estradiol, a known hormone and product of ABAD activity. Furthermore, AG18051 is protective against Aβ42 toxicity, as measured by LDH release and MTT absorbance. Specifically, AG18051 reduced Aβ42-induced impairment of mitochondrial respiration and oxidative stress as shown by reduced ROS (reactive oxygen species) levels. Guided by our previous finding of shared aspects of the toxicity of Aβ and human amylin (HA), with the latter forming aggregates in Type 2 diabetes mellitus (T2DM) pancreas, we determined whether AG18051 would also confer protection from HA toxicity. We found that the inhibitor conferred only partial protection from HA toxicity indicating distinct pathomechanisms of the two amyloidogenic agents. Taken together, our results present the inhibition of ABAD by compounds such as AG18051 as a promising therapeutic strategy for the prevention and treatment of AD, and suggest levels of estradiol as a suitable read-out

Modes of Aβ toxicity in Alzheimer’s disease

Alzheimer’s disease (AD) is reaching epidemic proportions, yet a cure is not yet available. While the genetic causes of the rare familial inherited forms of AD are understood, the causes of the sporadic forms of the disease are not. Histopathologically, these two forms of AD are indistinguishable: they are characterized by amyloid-β (Aβ) peptide-containing amyloid plaques and tau-containing neurofibrillary tangles. In this review we compare AD to frontotemporal dementia (FTD), a subset of which is characterized by tau deposition in the absence of overt plaques. A host of transgenic animal AD models have been established through the expression of human proteins with pathogenic mutations previously identified in familial AD and FTD. Determining how these mutant proteins cause disease in vivo should contribute to an understanding of the causes of the more frequent sporadic forms. We discuss the insight transgenic animal models have provided into Aβ and tau toxicity, also with regards to mitochondrial function and the crucial role tau plays in mediating Aβ toxicity. We also discuss the role of miRNAs in mediating the toxic effects of the Aβ peptide

Functional genomic screen and network analysis reveal novel modifiers of tauopathy dissociated from tau phosphorylation

A functional genetic screen using loss-of-function and gain-of-function alleles was performed to identify modifiers of tau-induced neurotoxicity using the 2N/4R (full-length) isoform of wild-type human tau expressed in the fly retina. We previously reported eye pigment mutations, which create dysfunctional lysosomes, as potent modifiers; here, we report 37 additional genes identified from ∼1900 genes screened, including the kinases shaggy/GSK-3beta, par-1/MARK, CamKI and Mekk1. Tau acts synergistically with Mekk1 and p38 to down-regulate extracellular regulated kinase activity, with a corresponding decrease in AT8 immunoreactivity (pS202/T205), suggesting that tau can participate in signaling pathways to regulate its own kinases. Modifiers showed poor correlation with tau phosphorylation (using the AT8, 12E8 and AT270 epitopes); moreover, tested suppressors of wild-type tau were equally effective in suppressing toxicity of a phosphorylation-resistant S11A tau construct, demonstrating that changes in tau phosphorylation state are not required to suppress or enhance its toxicity. Genes related to autophagy, the cell cycle, RNA-associated proteins and chromatin-binding proteins constitute a large percentage of identified modifiers. Other functional categories identified include mitochondrial proteins, lipid trafficking, Golgi proteins, kinesins and dynein and the Hsp70/Hsp90-organizing protein (Hop). Network analysis uncovered several other genes highly associated with the functional modifiers, including genes related to the PI3K, Notch, BMP/TGF-β and Hedgehog pathways, and nuclear trafficking. Activity of GSK-3β is strongly upregulated due to TDP-43 expression, and reduced GSK-3β dosage is also a common suppressor of Aβ42 and TDP-43 toxicity. These findings suggest therapeutic targets other than mitigation of tau phosphorylation

Dissecting toxicity of tau and beta-amyloid

How beta-amyloid (Abeta) and tau exert toxicity in Alzheimer's disease is only partly understood. Major questions include (1) which aggregation state of Abeta confers toxicity, (2) do amyloidogenic proteins have similar mechanisms of toxicity, and (3) does soluble tau interfere with cellular functions

Reflective Writing in Teacher Education in China: Insights from Systemic Functional Linguistics

This article aims to demonstrate the application of theory to teaching practice by examining how two teacher educators drew upon systemic functional linguistics (SFL) as a pedagogical and analytical tool to inform their teaching of reflective writing to Mandarin-dominant teacher candidates enrolled in an ESOL course within an educator preparation program at a university using English Medium Instruction (EMI) in China. First, the authors describe how they incorporated the SFL appraisal framework into their teaching to bring their multilingual student writers’ attention to the language of evaluation as they prepared to construct reflective language learning autobiographies. Second, the authors demonstrate how SFL-informed text analysis of the appraisal resources used within students’ written reflections deepened their understanding of their students’ reflective writing practices and informed their teaching and course development. The article concludes with suggestions for using the SFL appraisal framework to support the reflective writing of their multilingual teacher candidates

Tau physiology and pathomechanisms in frontotemporal lobar degeneration

Frontotemporal lobar degeneration (FTLD) has been associated with toxic intracellular aggregates of hyperphosphorylated tau (FTLD-tau). Moreover, genetic studies identified mutations in the MAPT gene encoding tau in familial cases of the disease. In this review, we cover a range of aspects of tau function, both in the healthy and diseased brain, discussing several in\ua0vitro and in\ua0vivo models. Tau structure and function in the healthy brain is presented, accentuating its distinct compartmentalization in neurons and its role in microtubule stabilization and axonal transport. Furthermore, tau-driven pathology is discussed, introducing current concepts and the underlying experimental evidence. Different aspects of pathological tau phosphorylation, the protein's genomic and domain organization as well as its spreading in disease, together with MAPT-associated mutations and their respective models are presented. Dysfunction related to other post-transcriptional modifications and their effect on normal neuronal functions such as cell cycle, epigenetics and synapse dynamics are also discussed, providing a mechanistic explanation for the observations made in FTLD-tau cases, with the possibility for therapeutic intervention. In this review, we cover aspects of tau function, both in the healthy and diseased brain, referring to different in\ua0vitro and in\ua0vivo models. In healthy neurons, tau is compartmentalized, with higher concentrations found in the distal part of the axon. Cargo molecules are sensitive to this gradient. A disturbed tau distribution, as found in frontotemporal lobar degeneration (FTLD-tau), has severe consequences for cellular physiology: tau accumulates in the neuronal soma and dendrites, leading among others to microtubule depolymerization and impaired axonal transport. Tau forms insoluble aggregates that sequester additional molecules stalling cellular physiology. Neuronal communication is gradually lost as toxic tau accumulates in dendritic spines with subsequent degeneration of synapses and synaptic loss. Thus, by providing a mechanistic explanation for the observations made in FTLD-tau cases, arises a possibility for therapeutic interventions. This article is part of the\ua0Frontotemporal Dementia special issue