Effects of Metacognitive Monitoring on Academic Achievement in an Ill-Structured Problem-Solving Environment

Higher education courses are increasingly moving online while educational approaches are concurrently shifting their focus toward student-centered approaches to learning. These approaches promote critical thinking by asking students to solve a range of ill-structured problems that exist in the real world. Researchers have found that student-centered online learning environments require students to have self-regulated learning skills, including metacognitive skills to regulate their own learning processes. Much of the research suggests that externally supporting students while they are learning online, either directly or indirectly, helps them to succeed academically. However, few empirical studies have investigated what levels of support are most effective for promoting students\u27 self-regulated learning behaviors. Additionally, these studies reported conflicting results – some found maximum support to be most effective while others found no significant difference. The purpose of this study was to investigate the effectiveness of different levels of support for self-regulated learning during a complex learning activity to solve an ill-structured problem-solving situation in an online learning environment. In addition, the role of students\u27 self-efficacy on their academic achievement was examined. A total of 101 undergraduate students from three international studies courses offered at a large urban Southeastern public university in the United States participated in the study. The students were randomly assigned to treatment (minimum support, maximum support) and control groups. Students\u27 academic achievement scores were measured using a conceptual knowledge test created by the professor teaching the courses. O\u27Neil\u27s (1997) Trait Self-Regulation Questionnaire measured students\u27 self-efficacy. Analysis of Co-Variance (ANCOVA) was conducted to analyze the data. The ANCOVA results indicated significant improvement of the academic achievement of the minimum support group versus both the maximum support and control groups. Additionally, self-efficacy as a co-variable did not significantly impact students\u27 achievement scores in any of the groups. The overall results indicated that it is important to consider the level of self-regulated learning support when designing online learning environments promoting students\u27 critical thinking skills. Promoting students\u27 self-regulated learning skills is vital when designing online higher education courses

A constant struggle : a history of deaf education in New South Wales since World War II

University of Technology Sydney. Faculty of Arts and Social Sciences.Despite developments in legislation, policy, advocacy and technology, all designed to improve deaf education and its delivery, Deaf, deaf, hard of hearing and hearing-impaired (DdHHHI) students still face a raft of issues from their early years of education through secondary high school. This thesis argues that, while there have been improvements, that situation continues due largely to fragmentation within the DdHHHI movement based on competing advocation for differing approaches to deaf education. This has occurred in the context of growing corporatisation and privatisation. The main area of difference has centered on how young DdHHHI people should learn, be it informal learning – in the home, the playground and the like – or formal learning – such as in the classroom. Should they be taught using oralism – teaching via spoken language – or manualism – teaching via sign language? The debate between oralism and manualism has had a significant impact on the type of education delivered to DdHHHI students in New South Wales (NSW). Deaf education has generally been affected by the choice of speech or sign, each being a communication mode that encapsulates its own unique languages. Since the 1960s, this situation has become more contested and increasingly pronounced. Different models of disability have come and gone. The findings of various inquiries and reports have stimulated various exchanges, though they have been implemented either in an ad hoc manner or not at all. New technologies have been introduced, heralding different methods of educating DdHHHI students with particular regard to their individual abilities and to their differing degrees of hearing loss. The debate further deepened with the introduction of bilingualism as another educational method in the early 1990s. Disability discrimination legislation and the United Nations’ Convention on the Rights of Persons with Disabilities served to further drive the deaf education debate. These required countries to take measures to facilitate the learning of sign language and ensure the education of DdHHHI children be delivered in the most appropriate languages, modes and means of communication for the individual and in environments that maximise academic and social development. However, DdHHHI students continue to be marginalised in the NSW education system

Predicting Impacts of Climate Change on Fasciola hepatica Risk

Fasciola hepatica (liver fluke) is a physically and economically devastating parasitic trematode whose rise in recent years has been attributed to climate change. Climate has an impact on the free-living stages of the parasite and its intermediate host Lymnaea truncatula, with the interactions between rainfall and temperature having the greatest influence on transmission efficacy. There have been a number of short term climate driven forecasts developed to predict the following season's infection risk, with the Ollerenshaw index being the most widely used. Through the synthesis of a modified Ollerenshaw index with the UKCP09 fine scale climate projection data we have developed long term seasonal risk forecasts up to 2070 at a 25 km square resolution. Additionally UKCIP gridded datasets at 5 km square resolution from 1970-2006 were used to highlight the climate-driven increase to date. The maps show unprecedented levels of future fasciolosis risk in parts of the UK, with risk of serious epidemics in Wales by 2050. The seasonal risk maps demonstrate the possible change in the timing of disease outbreaks due to increased risk from overwintering larvae. Despite an overall long term increase in all regions of the UK, spatio-temporal variation in risk levels is expected. Infection risk will reduce in some areas and fluctuate greatly in others with a predicted decrease in summer infection for parts of the UK due to restricted water availability. This forecast is the first approximation of the potential impacts of climate change on fasciolosis risk in the UK. It can be used as a basis for indicating where active disease surveillance should be targeted and where the development of improved mitigation or adaptation measures is likely to bring the greatest benefits

Olfactory testing does not predict β-amyloid, MRI measures of neurodegeneration or vascular pathology in the British 1946 birth cohort.

OBJECTIVE: To explore the value of olfactory identification deficits as a predictor of cerebral β-amyloid status and other markers of brain health in cognitively normal adults aged ~ 70 years. METHODS: Cross-sectional observational cohort study. 389 largely healthy and cognitively normal older adults were recruited from the MRC National Survey of Health and Development (1946 British Birth cohort) and investigated for olfactory identification deficits, as measured by the University of Pennsylvania Smell Identification Test. Outcome measures were imaging markers of brain health derived from 3 T MRI scanning (cortical thickness, entorhinal cortex thickness, white matter hyperintensity volumes); 18F florbetapir amyloid-PET scanning; and cognitive testing results. Participants were assessed at a single centre between March 2015 and January 2018. RESULTS: Mean (± SD) age was 70.6 (± 0.7) years, 50.8% were female. 64.5% had hyposmia and 2.6% anosmia. Olfaction showed no association with β-amyloid status, hippocampal volume, entorhinal cortex thickness, AD signature cortical thickness, white matter hyperintensity volume, or cognition. CONCLUSION AND RELEVANCE: In the early 70s, olfactory function is not a reliable predictor of a range of imaging and cognitive measures of preclinical AD. Olfactory identification deficits are not likely to be a useful means of identifying asymptomatic amyloidosis. Further studies are required to assess if change in olfaction may be a proximity marker for the development of cognitive impairment

Amyloid ? influences the relationship between cortical thickness and vascular load.

INTRODUCTION: Cortical thickness has been proposed as a biomarker of Alzheimer's disease (AD)- related neurodegeneration, but the nature of its relationship with amyloid beta (A?) deposition and white matter hyperintensity volume (WMHV) in cognitively normal adults is unclear. METHODS: We investigated the influences of A? status (negative/positive) and WMHV on cortical thickness in 408 cognitively normal adults aged 69.2 to 71.9 years who underwent 18F-Florbetapir positron emission tomography (PET) and structural magnetic resonance imaging (MRI). Two previously defined Alzheimer's disease (AD) cortical signature regions and the major cortical lobes were selected as regions of interest (ROIs) for cortical thickness. RESULTS: Higher WMHV, but not A? status, predicted lower cortical thickness across all participants, in all ROIs. Conversely, when A?-positive participants were considered alone, higher WMHV predicted higher cortical thickness in a temporal AD-signature region. DISCUSSION: WMHV may differentially influence cortical thickness depending on the presence or absence of A?, potentially reflecting different pathological mechanisms

Investigating associations between blood metabolites, later life brain imaging measures, and genetic risk for Alzheimer’s disease

BACKGROUND: Identifying blood-based signatures of brain health and preclinical pathology may offer insights into early disease mechanisms and highlight avenues for intervention. Here, we systematically profiled associations between blood metabolites and whole-brain volume, hippocampal volume, and amyloid-β status among participants of Insight 46-the neuroscience sub-study of the National Survey of Health and Development (NSHD). We additionally explored whether key metabolites were associated with polygenic risk for Alzheimer's disease (AD). METHODS: Following quality control, levels of 1019 metabolites-detected with liquid chromatography-mass spectrometry-were available for 1740 participants at age 60-64. Metabolite data were subsequently clustered into modules of co-expressed metabolites using weighted coexpression network analysis. Accompanying MRI and amyloid-PET imaging data were present for 437 participants (age 69-71). Regression analyses tested relationships between metabolite measures-modules and hub metabolites-and imaging outcomes. Hub metabolites were defined as metabolites that were highly connected within significant (pFDR < 0.05) modules or were identified as a hub in a previous analysis on cognitive function in the same cohort. Regression models included adjustments for age, sex, APOE genotype, lipid medication use, childhood cognitive ability, and social factors. Finally, associations were tested between AD polygenic risk scores (PRS), including and excluding the APOE region, and metabolites and modules that significantly associated (pFDR < 0.05) with an imaging outcome (N = 1638). RESULTS: In the fully adjusted model, three lipid modules were associated with a brain volume measure (pFDR < 0.05): one enriched in sphingolipids (hippocampal volume: ß = 0.14, 95% CI = [0.055,0.23]), one in several fatty acid pathways (whole-brain volume: ß =  - 0.072, 95%CI = [- 0.12, - 0.026]), and another in diacylglycerols and phosphatidylethanolamines (whole-brain volume: ß =  - 0.066, 95% CI = [- 0.11, - 0.020]). Twenty-two hub metabolites were associated (pFDR < 0.05) with an imaging outcome (whole-brain volume: 22; hippocampal volume: 4). Some nominal associations were reported for amyloid-β, and with an AD PRS in our genetic analysis, but none survived multiple testing correction. CONCLUSIONS: Our findings highlight key metabolites, with functions in membrane integrity and cell signalling, that associated with structural brain measures in later life. Future research should focus on replicating this work and interrogating causality

Comparison of artemether-lumefantrine and chloroquine with and without primaquine for the treatment of Plasmodium vivax infection in Ethiopia: A randomized controlled trial

Background: Recent efforts in malaria control have resulted in great gains in reducing the burden of Plasmodium falciparum, but P. vivax has been more refractory. Its ability to form dormant liver stages confounds control and elimination efforts. To compare the efficacy and safety of primaquine regimens for radical cure, we undertook a randomized controlled trial in Ethiopia. Methods and findings: Patients with normal glucose-6-phosphate dehydrogenase status with symptomatic P. vivax mono-infection were enrolled and randomly assigned to receive either chloroquine (CQ) or artemether-lumefantrine (AL), alone or in combination with 14 d of semi-supervised primaquine (PQ) (3.5 mg/kg total). A total of 398 patients (n = 104 in the CQ arm, n = 100 in the AL arm, n = 102 in the CQ+PQ arm, and n = 92 in the AL+PQ arm) were followed for 1 y, and recurrent episodes were treated with the same treatment allocated at enrolment. The primary endpoints were the risk of P. vivax recurrence at day 28 and at day 42. The risk of recurrent P. vivax infection at day 28 was 4.0% (95% CI 1.5%–10.4%) after CQ treatment and 0% (95% CI 0%–4.0%) after CQ+PQ. The corresponding risks were 12.0% (95% CI 6.8%–20.6%) following AL alone and 2.3% (95% CI 0.6%–9.0%) following AL+PQ. On day 42, the risk was 18.7% (95% CI 12.2%–28.0%) after CQ, 1.2% (95% CI 0.2%–8.0%) after CQ+PQ, 29.9% (95% CI 21.6%–40.5%) after AL, and 5.9% (95% CI 2.4%–13.5%) after AL+PQ (overall p < 0.001). In those not prescribed PQ, the risk of recurrence by day 42 appeared greater following AL treatment than CQ treatment (HR = 1.8 [95% CI 1.0–3.2]; p = 0.059). At the end of follow-up, the incidence rate of P. vivax was 2.2 episodes/person-year for patients treated with CQ compared to 0.4 for patients treated with CQ+PQ (rate ratio: 5.1 [95% CI 2.9–9.1]; p < 0.001) and 2.3 episodes/person-year for AL compared to 0.5 for AL+PQ (rate ratio: 6.4 [95% CI 3.6–11.3]; p < 0.001). There was no difference in the occurrence of adverse events between treatment arms. The main limitations of the study were the early termination of the trial and the omission of haemoglobin measurement after day 42, resulting in an inability to estimate the cumulative risk of anaemia. Conclusions: Despite evidence of CQ-resistant P. vivax, the risk of recurrence in this study was greater following treatment with AL unless it was combined with a supervised course of PQ. PQ combined with either CQ or AL was well tolerated and reduced recurrence of vivax malaria by 5-fold at 1 y

Neuroimaging, clinical and life course correlates of normal-appearing white matter integrity in 70-year-olds

We investigate associations between normal-appearing white matter (NAWM) microstructural integrity in cognitively normal ∼70-year-olds and concurrently measured brain health and cognition, demographics, genetics and life course cardiovascular health. Participants born in the same week in March 1946 (British 1946 Birth cohort) underwent PET-MRI around age 70. Mean standardized NAWM integrity metrics (fractional anisotropy (FA), mean diffusivity (MD), neurite density index (NDI) and orientation dispersion index (ODI)) were derived from diffusion MRI. Linear regression was used to test associations between NAWM metrics and (1) concurrent measures, including whole brain volume, white matter hyperintensity volume (WMHV), PET amyloid and cognition; (2) the influence of demographic and genetic predictors, including sex, childhood cognition, education, socioeconomic position, and genetic risk for Alzheimer’s Disease (APOE-ε4); (3) systolic and diastolic blood pressure and cardiovascular health (FHS-CVS) across adulthood. Sex interactions were tested. Statistical significance included false discovery rate correction (5%). 362 participants met inclusion criteria (mean age 70 years, 49% female). Higher WMHV was associated with lower FA (b=-0.09 [95%CI:-0.11, -0.06] p&amp;lt;0.01), NDI (b=-0.17 [-0.22, -0.12] p&amp;lt;0.01), and higher MD (b=0.14 [-0.10, -0.17] p&amp;lt;0.01); amyloid (in men) was associated with lower FA (b=-0.04 [-0.08, -0.01] p=0.03) and higher MD (b=0.06 [0.01,0.11] p=0.02). FHS-CVS in later-life (age 69) was associated with NAWM [lower FA (b=-0.06 [-0.09, -0.02] p&amp;lt;0.01), NDI (b=-0.10 [-0.17, -0.03] p&amp;lt;0.01), and higher MD (b=0.09 [0.04,0.14] p&amp;lt;0.01). Significant sex interactions (p&amp;lt;0.05) emerged for midlife cardiovascular health (age 53) and NAWM at 70: marginal effect plots demonstrated, in women only, NAWM was associated with higher midlife FHS-CVS (lower FA and NDI), midlife systolic (lower FA, NDI, and higher MD), and diastolic (lower FA and NDI) blood pressure, and greater blood pressure change between 43 and 53 years (lower FA and NDI), independently of WMHV. In summary, poorer NAWM microstructural integrity in ∼70-year-olds was associated with measures of cerebral small vessel disease, amyloid (in males) and later-life cardiovascular health, demonstrating how NAWM can provide additional information to overt white matter disease. Our findings further show that greater midlife cardiovascular risk and higher blood pressure were associated with poorer NAWM microstructural integrity in females only, suggesting that women’s brains may be more susceptible to the effects of midlife blood pressure and cardiovascular health

Associations of β-Amyloid and Vascular Burden With Rates of Neurodegeneration in Cognitively Normal Members of the 1946 British Birth Cohort

OBJECTIVE: To quantify the independent and interactive associations of amyloid-β (Aβ) and white matter hyperintensity volume (WMHV) - a marker of presumed cerebrovascular disease (CVD) - with rates of neurodegeneration, and to examine the contributions of APOE ε4 and vascular risk measured at different stages of adulthood in cognitively normal members of the 1946 British birth cohort. METHODS: Participants underwent brain MRI and florbetapir-Aβ positron emission tomography as part of Insight 46, an observational population-based study. Changes in whole brain, ventricular and hippocampal volume were directly measured from baseline and repeat volumetric T1 MRI using the Boundary Shift Integral. Linear regression was used to test associations with: baseline Aβ deposition; baseline WMHV; APOE ε4; and office-based Framingham heart study-cardiovascular risk scores (FHS-CVS) and systolic blood pressure (BP) at ages 36, 53 and 69 years. RESULTS: 346 cognitively normal participants (mean [SD] age at baseline scan 70.5 [0.6] years; 48% female) had high-quality T1 MRI data from both time-points (mean [SD] scan interval 2.4 [0.2] years). Being Aβ positive at baseline was associated with 0.87 ml/year faster whole brain atrophy (95% CI 0.03, 1.72), 0.39 ml/year greater ventricular expansion (95% CI 0.16, 0.64) and 0.016 ml/year faster hippocampal atrophy (95% CI 0.004, 0.027), while each 10 ml additional WMHV at baseline was associated with 1.07 ml/year faster whole brain atrophy (95% CI 0.47, 1.67), 0.31 ml/year greater ventricular expansion (95% CI 0.13, 0.60) and 0.014 ml/year faster hippocampal atrophy (95% CI 0.006, 0.022). These contributions were independent and there was no evidence that Aβ and WMHV interacted in their effects. There were no independent associations of APOE ε4 with rates of neurodegeneration after adjusting for Aβ status and WMHV, and no clear relationships between FHS-CVS or systolic BP and rates of neurodegeneration when assessed across the whole sample, nor any evidence that they acted synergistically with Aβ. CONCLUSIONS: Aβ and presumed CVD have distinct and additive effects on rates of neurodegeneration in cognitively normal elderly. These findings have implications for the use of MRI measures as biomarkers of neurodegeneration and emphasize the importance of risk management and early intervention targeting both pathways