Comparing Two CBM Maze Selection Tools: Considering Scoring and Interpretive Metrics for Universal Screening

Advances in maze selection curriculum-based measurement (CBM) have led to several published tools with technical information for interpretation (e.g., norms, benchmarks, cut-scores, classification accuracy) that have increased their usefulness for universal screening. A range of scoring practices have emerged for evaluating student performance on maze selection (e.g., correct restoration, incorrect restoration, correct restoration minus incorrect restoration, and correct restoration minus one-half incorrect restoration). However, lack of clear understanding about the intersection between scoring and interpretation has resulted in limited evidence about using maze selection for making universal screening decisions. In this study, 925 students in Grades 3-6 completed two CBMs for maze selection. Student performance on the two was compared across different scoring metrics. Limitations and practical implications are discussed

Examining Oral Passage Reading Rate Across Three Curriculum-Based Measurement Tools for Predicting Grade-Level Proficiency

Curriculum-based measurement (CBM) for oral passage reading (OPR) is among the most commonly used tools for making screening decisions regarding academic proficiency status for students in first through sixth grades. Multiple publishers make available OPR tools, and while they are designed to measure the same broad construct of reading, research suggests that student performance varies within grades and across publishers. Despite the existence of multiple publishers of CBM tools for OPR, many of which include publisher-specific recommendations comparing student performance to a proficiency standard, the use of normative-based cut scores to interpret student performance remains prevalent. In the current study, three commercially available CBM tools for OPR were administered to 1,482 students in first through sixth grade. Results suggest differences between normative- and criterion-based approaches to determining cut scores for screening decisions. Implications regarding resource allocation for students in need of additional intervention are discussed

Sexual Health after a Breast Cancer Diagnosis: Addressing a Forgotten Aspect of Survivorship

Breast cancer is the most common cancer in women. The life expectancy after a breast cancer diagnosis is improving steadily, leaving many more persons with the long-term consequences of treatment. Sexual problems are a common concern for breast cancer survivors yet remain overlooked in both the clinical setting and the research literature. Factors that contribute to sexual health concerns in breast cancer survivors are biopsychosocial, as are the barriers to addressing and treating these health concerns. Sexual health needs and treatment may vary by anatomy and gender. Multidisciplinary management may comprise lifestyle modifications, medications, sexual health aids such as vibrators, counseling, and referrals to pelvic health physical therapy and specialty care. In this article, we review the contributing factors, screening, and management of sexual difficulties in cisgender female breast cancer survivors. More information is needed to better address the sexual health of breast cancer survivors whose sexual/gender identity differs from that of cisgender women

Gut microbiota–specific IgA+ B cells traffic to the CNS in active multiple sclerosis

Changes in gut microbiota composition and a diverse role of B cells have recently been implicated in multiple sclerosis (MS), a central nervous system (CNS) autoimmune disease. Immunoglobulin A (IgA) is a key regulator at the mucosal interface. However, whether gut microbiota shape IgA responses and what role IgA+ cells have in neuroinflammation are unknown. Here, we identify IgA-bound taxa in MS and show that IgA-producing cells specific for MS-associated taxa traffic to the inflamed CNS, resulting in a strong, compartmentalized IgA enrichment in active MS and other neuroinflammatory diseases. Unlike previously characterized polyreactive anti-commensal IgA responses, CNS IgA cross-reacts with surface structures on specific bacterial strains but not with brain tissue. These findings establish gut microbiota-specific IgA+ cells as a systemic mediator in MS and suggest a critical role of mucosal B cells during active neuroinflammation with broad implications for IgA as an informative biomarker and IgA-producing cells as an immune subset to harness for therapeutic interventions

Stratifying the presymptomatic phase of genetic frontotemporal dementia by Serum NfL and pNfH: a longitudinal multicentre study

© 2021 The Authors. Annals of Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.Objective: Although the presymptomatic stages of frontotemporal dementia (FTD) provide a unique chance to delay or even prevent neurodegeneration by early intervention, they remain poorly defined. Leveraging a large multicenter cohort of genetic FTD mutation carriers, we provide a biomarker-based stratification and biomarker cascade of the likely most treatment-relevant stage within the presymptomatic phase: the conversion stage. Methods: We longitudinally assessed serum levels of neurofilament light (NfL) and phosphorylated neurofilament heavy (pNfH) in the Genetic FTD Initiative (GENFI) cohort (n = 444), using single-molecule array technique. Subjects comprised 91 symptomatic and 179 presymptomatic subjects with mutations in the FTD genes C9orf72, GRN, or MAPT, and 174 mutation-negative within-family controls. Results: In a biomarker cascade, NfL increase preceded the hypothetical clinical onset by 15 years and concurred with brain atrophy onset, whereas pNfH increase started close to clinical onset. The conversion stage was marked by increased NfL, but still normal pNfH levels, while both were increased at the symptomatic stage. Intra-individual change rates were increased for NfL at the conversion stage and for pNfH at the symptomatic stage, highlighting their respective potential as stage-dependent dynamic biomarkers within the biomarker cascade. Increased NfL levels and NfL change rates allowed identification of presymptomatic subjects converting to symptomatic disease and capture of proximity-to-onset. We estimate stage-dependent sample sizes for trials aiming to decrease neurofilament levels or change rates. Interpretation: Blood NfL and pNfH provide dynamic stage-dependent stratification and, potentially, treatment response biomarkers in presymptomatic FTD, allowing demarcation of the conversion stage. The proposed biomarker cascade might pave the way towards a biomarker-based precision medicine approach to genetic FTD..W. and M.S. are members of the European Reference Network for Rare Neurological Diseases Project ID No. 739510. This work was supported by the Horizon 2020 research and innovation program (grant 779257 Solve-RD to M.S.), the National Ataxia Foundation (grant to C.W. and M.S.), the Wilhelm Vaillant Stiftung (grant to C.W.), the EU Joint Programme – Neurodegenerative Disease Research (JPND) “GENFI-prox” through participating national funding agencies (by DLR/BMBF to M.S., J.D.R., B.B., C.G., and M.O.), and the European Union's Horizon 2020 research and innovation programme under grant agreement No. 643417. J.C.S. and H.S. received funding by two Memorabel grants from Deltaplan Dementie (The Netherlands Organisation for Health Research and Development and Alzheimer Nederland; grant numbers 733050813 and 733050103) in the Netherlands and the Bluefield Project to Cure Frontotemporal Dementia. J.B.R. was supported by the NIHR Cambridge Biomedical Research Centre (BRC-1215-20014) and the Medical Research Council (SUAG/051 G101400). C.B. is supported by a postdoctoral fellowship from the Swiss National Science Foundation (P400PM_191077). J.D.R. is supported by the Miriam Marks Brain Research UK Senior Fellowship and has received funding from an MRC Clinician Scientist Fellowship (MR/M008525/1) and the NIHR Rare Disease Translational Research Collaboration (BRC149/NS/MH). This work was also supported by the MRC UK GENFI grant (MR/M023664/1), the Bluefield Project and the JPND GENFI-PROX grant (2019-02248).info:eu-repo/semantics/publishedVersio