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Indigenous peoples represent approximately 5% of the world's population and reside in over 90 countries worldwide. They embody a rich diversity of cultures, traditions, languages and relationships with the land that are shared through many generations and that are distinct from those of the settler societies within which they now live. Many Indigenous peoples have a shared experience of discrimination, trauma, and violation of rights, rooted in complex sociopolitical relationships with settler societies that are still ongoing. This results in continuing social injustices and pronounced disparities in health for many Indigenous peoples around the globe. Indigenous peoples exhibit a significantly higher cancer incidence, mortality, and poorer survival compared to non-Indigenous peoples. Cancer services, including radiotherapy, have not been designed to support the specific values and needs of Indigenous populations, resulting in poorer access to cancer services for Indigenous peoples globally across the entire cancer care spectrum. Specific to radiotherapy, available evidence demonstrates disparities in radiotherapy uptake between Indigenous and non-Indigenous patients. Radiotherapy centres are also located disparately further away from Indigenous communities. Studies are limited by a lack of Indigenous-specific data to help inform effective radiotherapy delivery. Recent Indigenous-led partnerships and initiatives have helped to address existing gaps in cancer care, and radiation oncologists play an important role in supporting such efforts. In this article, we present an overview of access to radiotherapy for Indigenous peoples in Canada and Australia, with a focus on strengthening cancer care delivery through education, partnerships, and research.

Our words are powerful and can influence others’ perceptions, attitudes, and behaviours. Published research is no exception to this. Historically, much of the research involving Indigenous Peoples has been exploitative, contributing to inequities instead of resolving them (Ermine et al., 2004; Greenwood et al., 2018; Marsden et al., 2020). While recent research publications tend to use more inclusive terminology, more subtle instances of bias, stereotyping or paternalistic language are as dangerous and influential as more overt examples of racism. An example of hidden bias can be found in the deficit-based nature of much Western-based research methodology. This deficit thinking, when applied repeatedly to Indigenous populations and certain topics, runs the risk of perpetually associating Indigeneity with notions of problems, fault, and scarcity. This is especially true if researchers do not contextualize the issue by engaging in a discussion of colonization, therefore telling only one side of a complex story (Fogarty et al., 2018). Deficit-based research can thus erode the protective factors of the very communities that it is attempting to serve (Resiliency Initiatives, 2013). Disengaging from deficit thinking in research involving Indigenous Peoples is therefore essential to affecting change. Strengths-based approaches may provide a solution (Askew et al., 2020). While these approaches recognize the challenges Indigenous Peoples face, they focus on and leverage the inherent strengths, capacities, and self-determination of Indigenous Peoples. In emphasizing the empowerment and support of their strengths, strengths-based approaches aim to create new narratives to disrupt the existing deficit discourse (Bryant et al., 2021). A number of published guidelines and studies outline strengths-based methods for conducting Indigenous research ‘with’ and not ‘on’ Indigenous Peoples (Hayward et al., 2021; Huria et al., 2019; Welch et al., 2012). These guidelines tend to focus on important topics such as community-based participatory research, authentic partnering and engagement, data ownership, control of the research, and data access and storage (Hayward et al., 2021). While principles and protocols which respect community ownership, control, access and possession, such as OCAP® (First Nations Information Governance Centre, 2015), for example, are essential, guidance for disseminating research and writing which respects Indigenous communities is needed for knowledge translation. Our scoping review aims to identify articles that focus on the discourse of how Indigenous Peoples are represented in the scholarly literature. While Gregory Younging (Younging, 2018) and Chelsea Vowel (Vowel, 2016) have published guides accepted in the social sciences, this scoping review will identify articles which focus on analyzing or describing bias in academic writing beyond Indigenous Studies and Indigenous literary works to encompass and be inclusive of academic publishing in interdisciplinary fields, including the sciences.

Infographic resource providing tips for educational professionals conducting reading assessment with multilingual children. Resources are based on "Assessing Oral Language when Screening Multilingual Children for Reading Disabilities", an invited manuscript for a special issue in Intervention in School and Clinic. Designs by C. J. Davis.

The present study will examine the contributions of language ability and word reading ability to math performance in Grade 2 children.

Additional file 1. Results of post hoc Bonferroni test for relative declines in different regional body parts.

Aim: To understand miRNA changes across gestation in healthy human placentae. This is essential before miRNAs can be used as biomarkers or prognostic indicators during pregnancy. Materials & methods: Using next-generation sequencing, we characterize the normative human placenta miRNome in first (n =113) and third trimester (n =47). Results &conclusion: There are 801 miRNAs expressed in both first and third trimester, including 182 with similar expression across gestation (p ≥0.05, foldchange ≤2) and 180 significantly different (false discovery rate 2). Of placenta-specific miRNA clusters, chromosome 14 miRNA cluster decreases across gestation and chromosome 19miRNA cluster is overall highly expressed. Chromosome 13 clusters are upregulated in first trimester. This work provides a rich atlas of healthy pregnancies to direct functional studies investigating the epigenetic differences in first and third trimester placentae.

The conserved transmembrane receptor Notch has diverse and profound roles in controlling cell fate during animal development. In the absence of ligand, a Negative Regulatory Region (NRR) in the Notch ectodomain adopts an autoinhibited confirmation, masking an ADAM protease cleavage site(1,2); ligand binding induces cleavage of the NRR, leading to Notch ectodomain shedding as the first step of signal transduction(3,4). In Drosophila and vertebrates, recruitment of transmembrane Delta/Serrate/LAG-2 (DSL) ligands by the endocytic adaptor Epsin, and their subsequent internalization by Clathrin-mediated endocytosis exerts a “pulling force” on Notch that is essential to expose the cleavage site in the NRR(4–6). Here, we show that Epsin-mediated endocytosis of transmembrane ligands is not essential to activate the two C. elegans Notch proteins, LIN-12 and GLP-1. Using an in vivo force sensing assay in Drosophila(6), we present evidence (i) that the LIN-12 and GLP-1 NRRs are tuned to lower force thresholds than the NRR of Drosophila Notch, and (ii), that this difference depends on the absence of a “Leucine plug” that occludes the cleavage site in the Drosophila and vertebrate Notch NRRs(1,2). Our results thus establish an unexpected evolutionary plasticity in the force-dependent mechanism of Notch activation and implicate a specific structural element, the Leucine plug, as a determinant.

The LIN-12/Notch signaling pathway is highly conserved in all animals, and is crucial for proper development. It is a key pathway in specifying cell fate in many cellular contexts, and dysregulation of the pathway can have deleterious consequences. Therefore, understanding how LIN-12/Notch signaling is regulated in different contexts has been a main area of interest in the field. Previous studies in different model organisms have identified many modes of regulation of the signaling pathway, one of which is endocytosis of the ligand and receptor. Here, I further investigated the role of endocytosis in LIN-12/Notch signaling in multiple developmental contexts in Caenorhabditis elegans. Work in Drosophila and vertebrates had previously established that ligand-mediated activation of Notch requires ubiquitination of the intracellular domain of the transmembrane ligand and the activity of the endocytic adaptor Epsin in the signaling cell. The consensus in the field is that Epsin-mediated endocytosis of mono-ubiquitinated ligand generates a pulling force that exposes a cleavage site in Notch for an ADAM protease, a critical step in signal transduction. In contrast, in this thesis, I examined two different transmembrane ligands in several different cell contexts and found that activation of LIN-12/Notch and the paralogous GLP-1/Notch in C. elegans does not require either Epsin-mediated endocytosis or ubiquitination of the intracellular domain of the ligand. Results obtained by a collaborator indicate that C. elegans ligand and receptor interactions are tuned to a lower force threshold than are Drosophila ligand and receptor interactions, potentially accounting for these differences. I also looked at the role of endocytosis in regulating LIN-12 signaling in the context of vulval development. The cell fate pattern of six vulval precursor cells (VPCs) is mediated by EGFR and LIN-12/Notch signaling. Previous work using multicopy transgenes in fixed specimens indicated that LIN-12 is post-translationally downregulated via endocytosis in response to EGFR activation in the VPC named P6.p, an event that appeared essential for ligands to activate LIN-12/Notch in neighboring VPCs. In this thesis, I manipulate the endogenous lin-12 gene and examine live specimens to show that LIN-12 appears to be regulated transcriptionally in P6.p and evidence that there may be additional potential endocytic motifs that may regulate LIN-12 in this context.

PurposeData have demonstrated an association between regret and lack of fertility counseling among patients undergoing treatment for non-gynecologic cancers. We sought to determine if fertility-related regret is reduced with pre-treatment counseling or fertility-sparing surgery (FSS) in patients with gynecologic cancers.MethodsA cross-sectional survey was administered to 593 reproductive-age survivors (18-40years old at diagnosis) of localized cervix, ovarian, or endometrial cancers that were eligible for FSS. A validated decision regret score was used to evaluate regret in patients.ResultsFour hundred seventy women completed the survey. Forty-six percent received pre-treatment counseling about treatment's effects on fertility. Having received counseling (adjusted ß-coefficient of -1.24, 95% CI = -2.29 to -0.18, p = 0.02), satisfactory counseling (adjusted ß-coefficient of -2.71, 95% CI = -3.86 to -1.57, p 0.05). While 50% of women reported desiring more children after diagnosis, desire for children after treatment was associated with increased regret (adjusted ß-coefficient of 3.97, 95% CI = 2.92-5.02, p

List of food categories with reference amount, serving size and FLIP data characteristics. This table outlines the food categories included in the paper along with the Schedule M reference amounts, CFIA suggested serving sizes and the number of products in the FLIP database that corresponded to each category. (DOCX 23 kb)

Long-term exposure to stress and its physiological mediators, in particular cortisol, may lead to impaired telomere maintenance. In this study, we examine if greater cortisol responses to an acute stressor and/or dysregulated patterns of daily cortisol secretion are associated with shorter telomere length. Twenty-three postmenopausal women comprising caregivers for dementia partners (n = 14) and age- and BMI-matched non-caregivers provided home sampling of cortisol-saliva samples at waking, 30. min after waking, and bedtime, and a 12-hour overnight urine collection. They were also exposed to an acute laboratory stressor throughout which they provided saliva samples. Peripheral blood mononuclear cells were isolated from a fasting blood sample and assayed for telomere length. As hypothesized, greater cortisol responses to the acute stressor were associated with shorter telomeres, as were higher overnight urinary free cortisol levels and flatter daytime cortisol slopes. While robust physiological responses to acute stress serve important functions, the long-term consequences of frequent high stress reactivity may include accelerated telomere shortening. © 2011 Elsevier Inc.