Therapists as Educators: the Importance of Client Education in Occupational Therapy

Client education is a major component of everyday health care practice. Entry-level occupational therapy (OT) accreditation standards require educators to teach students how to demonstrate the ability to educate clients, family, caregivers, and significant others to facilitate their skills related to personal occupations. Although these standards are a necessity, entry-level programs are not required to teach students the teaching methodologies that support human learning. However, the educational standards do require students to apply the principles of teaching and learning processes. This project explored the evidence in teaching and learning strategies and how these were introduced to OT students during their program. Faculty from the School of Occupational Therapy and School of Education developed a module for entry-level OT students. Data analysis found that students were able to benefit from the additional information on teaching and learning theory

Magnitude and determinants of change in objectively-measured physical activity, sedentary time and sleep duration from ages 15 to 17.5y in UK adolescents: the ROOTS study.

BACKGROUND: Self-reported physical activity (PA) and sleep duration (SLP) change markedly throughout adolescence. We sought to quantify changes in objectively-measured PA, sedentary time (ST) and SLP through adolescence, and to investigate baseline body composition and baseline activity levels as determinants of change. METHODS: Individually calibrated combined heart rate and movement sensing was used to estimate PA energy expenditure (PAEE), SLP, daily ST and time in light (LPA), moderate (MPA), vigorous (VPA), and moderate-to-vigorous physical activity (MVPA) in 144 adolescents (50% boys) of mean age 15.1(±0.3)y at baseline and 17.5(±0.3)y at follow-up. Changes in PA (ΔPA), ST (ΔST) and SLP (ΔSLP) were calculated as follow-up minus baseline values. Waist circumference (WC) was measured at baseline and follow-up, as was fat mass index (FMI) and fat-free mass index (FFMI) by a pooled estimation method including bio-impedance. Comparison of baseline and follow-up activity was made by mixed-model ANOVA. Linear regression adjusted for baseline demographics, total and weekend hours of monitor wear time and the seasons of activity measurements, was used to investigate baseline body composition as determinants of ΔPA, ΔST and ΔSLP. A further model adjusted for baseline of the outcome assessed baseline activity as a predictor of behaviour change, and investigated associations for baseline body composition independent of the baseline level of the outcome. RESULTS: From baseline to follow-up levels of MPA and VPA declined (p ≤ 0.039). The annual decline in MVPA was equivalent to -4.5 and -3.0 min/d in boys and girls, respectively. Baseline FMI, FFMI and WC were positively associated with ΔLPA and negatively associated with ΔST in boys when adjusted for baseline of the outcome (p ≤ 0.037 for all). SLP increased from baseline to follow-up (p = 0.004) but ΔSLP was not associated with baseline body composition (p ≥ 0.13). For all variables, higher baseline levels were associated with greater declines over time (p ≤ 0.003). CONCLUSIONS: Levels of higher-intensity PA decline from mid-to-late adolescence, whereas the duration of sleep increases. Changes in LPA and ST may be associated with baseline body composition, but the baseline level of the outcome is consistently the strongest predictor of changes in adolescent activity.This work was supported by the Medical Research Council [Unit Programme grant numbers MC_U106179476 and MC_UU_12015/3], the Wellcome Trust [grant 074296/ Z/04/Z] and the British Heart Foundation [grant FS/12/58/29709 to KWi].This is the final version. It was first published by Springer at http://link.springer.com/article/10.1186%2Fs12966-015-0222-4

Prospective associations between sedentary time, sleep duration and adiposity in adolescents.

OBJECTIVE: The objective of this study was to investigate whether objectively measured sedentary time and sleep duration are associated with changes in adiposity from mid- to late adolescence. METHODS: Students (n = 504, 42% boys) were recruited from schools in Cambridgeshire, UK. At baseline (mean age 15.0 ± 0.3 years), sedentary time was objectively measured by ≥3 days of combined heart rate and movement sensing. Concurrently, sleep duration was measured by combined sensing in conjunction with self-reported bed times. Fat mass index (FMI; kg/m(2)) was estimated at baseline and follow-up (17.5 ± 0.3 years) by anthropometry and bioelectrical impedance. FMI change (ΔFMI) was calculated by subtracting the baseline from follow-up values. Linear regression models adjusted for basic demographics, moderate-to-vigorous physical activity (MVPA), and depressive symptoms were used to investigate associations of sedentary time and sleep duration (mutually adjusted for one another) with ΔFMI. RESULTS: FMI increased by 0.5 and 0.6 kg/m(2) in boys and girls, respectively, but there was no association between sedentary time and ΔFMI in either gender (p ≥ 0.087), and no association between sleep duration and ΔFMI in girls (p ≥ 0.61). In boys, each additional hour of baseline sleep significantly reduced the ΔFMI by 0.13 kg/m(2) (p = 0.049), but there was little evidence for this association after adjusting for MVPA and depressive symptoms (p = 0.15). CONCLUSIONS: Sedentary time may not determine changes in adiposity from mid- to late adolescence, nor may sleep duration in girls. However, sleep length may be inversely associated with adiposity gain in boys, depending on whether the relationship is confounded or mediated by MVPA and depression.This work was supported by the Medical Research Council (Unit Programme number MC_UU_12015/3), the Wellcome Trust (grant 074296/Z/04/Z) and the British Heart Foundation (grant FS/12/58/29709 to KW).This is the final version of the article. It first appeared from Elsevier via http://dx.doi.org/10.1016/j.sleep.2015.02.53

Effects of polygenic risk for suicide attempt and risky behavior on brain structure in young people with familial risk of bipolar disorder

Bipolar disorder (BD) is associated with a 20–30-fold increased suicide risk compared to the general population. First-degree relatives of BD patients show inflated rates of psychopathology including suicidal behaviors. As reliable biomarkers of suicide attempts (SA) are lacking, we examined associations between suicide-related polygenic risk scores (PRSs)—a quantitative index of genomic risk—and variability in brain structures implicated in SA. Participants (n = 206; aged 12–30 years) were unrelated individuals of European ancestry and comprised three groups: 41 BD cases, 96 BD relatives (“high risk”), and 69 controls. Genotyping employed PsychArray, followed by imputation. Three PRSs were computed using genome-wide association data for SA in BD (SA-in-BD), SA in major depressive disorder (SA-in-MDD) (Mullins et al., 2019, The American Journal of Psychiatry, 176(8), 651–660), and risky behavior (Karlsson Linnér et al., 2019, Nature Genetics, 51(2), 245–257). Structural magnetic resonance imaging processing employed FreeSurfer v5.3.0. General linear models were constructed using 32 regions-of-interest identified from suicide neuroimaging literature, with false-discovery-rate correction. SA-in-MDD and SA-in-BD PRSs negatively predicted parahippocampal thickness, with the latter association modified by group membership. SA-in-BD and Risky Behavior PRSs inversely predicted rostral and caudal anterior cingulate structure, respectively, with the latter effect driven by the “high risk” group. SA-in-MDD and SA-in-BD PRSs positively predicted cuneus structure, irrespective of group. This study demonstrated associations between PRSs for suicide-related phenotypes and structural variability in brain regions implicated in SA. Future exploration of extended PRSs, in conjunction with a range of biological, phenotypic, environmental, and experiential data in high risk populations, may inform predictive models for suicidal behaviors.Australian National Health and Medical Research Council (NHMRC); Lansdowne Foundation, Paul and Jenny Reid, Good Talk, and the Keith Pettigrew Family Bequest. DNA extraction was undertaken by Genetic Repositories Australia (GRA; www.neura.edu.au/GRA), Claudio Toma is a recipient of a “Ramón y Cajal” fellowship (RYC2018-024106-I) from the Spanish MINECO. This research was undertaken with the assistance of resources from the National Computational Infrastructure (NCI), which is supported by the Australian Governmen

Discovery of a new generation of angiotensin receptor blocking drugs:Receptor mechanisms and in silico binding to enzymes relevant to SARS-CoV-2

The discovery and facile synthesis of a new class of sartan-like arterial antihypertensive drugs (angiotensin receptor blockers [ARBs]), subsequently referred to as “bisartans” is reported. In vivo results and complementary molecular modelling presented in this communication indicate bisartans may be beneficial for the treatment of not only heart disease, diabetes, renal dysfunction, and related illnesses, but possibly COVID-19. Bisartans are novel bis-alkylated imidazole sartan derivatives bearing dual symmetric anionic biphenyl tetrazole moieties. In silico docking and molecular dynamics studies revealed bisartans exhibited higher binding affinities for the ACE2/spike protein complex (PDB 6LZG) compared to all other known sartans. They also underwent stable docking to the Zn2+ domain of the ACE2 catalytic site as well as the critical interfacial region between ACE2 and the SARS-CoV-2 receptor binding domain. Additionally, semi-stable docking of bisartans at the arginine-rich furin-cleavage site of the SARS-CoV-2 spike protein (residues 681–686) required for virus entry into host cells, suggest bisartans may inhibit furin action thereby retarding viral entry into host cells. Bisartan tetrazole groups surpass nitrile, the pharmacophoric “warhead” of PF-07321332, in its ability to disrupt the cysteine charge relay system of 3CLpro. However, despite the apparent targeting of multifunctional sites, bisartans do not inhibit SARS-CoV-2 infection in bioassays as effectively as PF-07321332 (Paxlovid)

Childhood socioeconomic position and objectively measured physical capability levels in adulthood: a systematic review and meta-analysis

<p><b>Background:</b> Grip strength, walking speed, chair rising and standing balance time are objective measures of physical capability that characterise current health and predict survival in older populations. Socioeconomic position (SEP) in childhood may influence the peak level of physical capability achieved in early adulthood, thereby affecting levels in later adulthood. We have undertaken a systematic review with meta-analyses to test the hypothesis that adverse childhood SEP is associated with lower levels of objectively measured physical capability in adulthood.</p> <p><b>Methods and Findings:</b> Relevant studies published by May 2010 were identified through literature searches using EMBASE and MEDLINE. Unpublished results were obtained from study investigators. Results were provided by all study investigators in a standard format and pooled using random-effects meta-analyses. 19 studies were included in the review. Total sample sizes in meta-analyses ranged from N = 17,215 for chair rise time to N = 1,061,855 for grip strength. Although heterogeneity was detected, there was consistent evidence in age adjusted models that lower childhood SEP was associated with modest reductions in physical capability levels in adulthood: comparing the lowest with the highest childhood SEP there was a reduction in grip strength of 0.13 standard deviations (95% CI: 0.06, 0.21), a reduction in mean walking speed of 0.07 m/s (0.05, 0.10), an increase in mean chair rise time of 6% (4%, 8%) and an odds ratio of an inability to balance for 5s of 1.26 (1.02, 1.55). Adjustment for the potential mediating factors, adult SEP and body size attenuated associations greatly. However, despite this attenuation, for walking speed and chair rise time, there was still evidence of moderate associations.</p> <p><b>Conclusions:</b> Policies targeting socioeconomic inequalities in childhood may have additional benefits in promoting the maintenance of independence in later life.</p&gt

Does Birth Weight Influence Physical Activity in Youth? A Combined Analysis of Four Studies Using Objectively Measured Physical Activity

Animal models suggest growth restriction in utero leads to lower levels of motor activity. Furthermore, individuals with very low birth weight report lower levels of physical activity as adults. The aim of this study was to examine whether birth weight acts as a biological determinant of physical activity and sedentary time. This study uses combined analysis of three European cohorts and one from South America (n = 4,170). Birth weight was measured or parentally reported. Height and weight were measured and used to calculate Body Mass Index (BMI). PA was objectively measured using accelerometry for ≥3 days, ≥10 hours day. Data was standardized to allow comparisons between different monitors. Total physical activity was assessed as counts per minute (cpm), with time spent above moderate activity (MVPA) >2,000 counts and time spent sedentary (<100 counts). There was no evidence for an association between birth weight and total physical activity (p = 0.9) or MVPA (p = 0.7). Overall there was no evidence for an association between birth weight and sedentary time (p = 0.8). However in the Pelotas study we did find an association between higher birth weight (kg) and lower overall physical activity (cpm) (β = −31, 95%CI: −58, −46, p = 0.03) and higher birth weight and greater sedentary time (mins/day) (β = 16.4, 95%CI: 5.3, 27.5, p = 0.004), although this was attenuated and no longer significant with further adjustment for gestational age. Overall this combined analysis suggests that birth weight may not be an important biological determinant of habitual physical activity or sedentary behaviour in children and adolescents

A G358S mutation in the Plasmodium falciparum Na⁺ pump PfATP4 confers clinically-relevant resistance to cipargamin

Diverse compounds target the Plasmodium falciparum Na(+) pump PfATP4, with cipargamin and (+)-SJ733 the most clinically-advanced. In a recent clinical trial for cipargamin, recrudescent parasites emerged, with most having a G358S mutation in PfATP4. Here, we show that PfATP4(G358S) parasites can withstand micromolar concentrations of cipargamin and (+)-SJ733, while remaining susceptible to antimalarials that do not target PfATP4. The G358S mutation in PfATP4, and the equivalent mutation in Toxoplasma gondii ATP4, decrease the sensitivity of ATP4 to inhibition by cipargamin and (+)-SJ733, thereby protecting parasites from disruption of Na(+) regulation. The G358S mutation reduces the affinity of PfATP4 for Na(+) and is associated with an increase in the parasite’s resting cytosolic [Na(+)]. However, no defect in parasite growth or transmissibility is observed. Our findings suggest that PfATP4 inhibitors in clinical development should be tested against PfATP4(G358S) parasites, and that their combination with unrelated antimalarials may mitigate against resistance development

Beliefs About Medication and Uptake of Preventive Therapy in Women at Increased Risk of Breast Cancer: Results From a Multicenter Prospective Study

Introduction Uptake of preventive therapies for breast cancer is low. We examined whether women at increased risk of breast cancer can be categorized into groups with similar medication beliefs, and whether belief group membership was prospectively associated with uptake of preventive therapy. Patients and Methods Women (n = 732) attending an appointment to discuss breast cancer risk were approached; 408 (55.7%) completed the Beliefs About Medicines and the Perceived Sensitivity to Medicines questionnaires. Uptake of tamoxifen at 3 months was reported in 258 (63.2%). The optimal number of belief groups were identified using latent profile analysis. Results Uptake of tamoxifen was 14.7% (38/258). One in 5 women (19.4%; 78/402) reported a strong need for tamoxifen. The model fit statistics supported a 2-group model. Both groups held weak beliefs about their need for tamoxifen for current and future health. Group 2 (38%; 154/406 of the sample) reported stronger concerns about tamoxifen and medicines in general, and stronger perceived sensitivity to the negative effects of medicines compared with group 1 (62%; 252/406). Women with low necessity and lower concerns (group 1) were more likely to initiate tamoxifen (18.3%; 33/180) than those with low necessity and higher concerns (group 2) (6.4%; 5/78). After adjusting for demographic and clinical factors, the odds ratio was 3.37 (95% confidence interval, 1.08-10.51; P = .036). Conclusion Uptake of breast cancer preventive therapy was low. A subgroup of women reported low need for preventive therapy and strong medication concerns. These women were less likely to initiate tamoxifen. Medication beliefs are targets for supporting informed decision-making

mTORC1-mediated translational elongation limits intestinal tumour initiation and growth.

Inactivation of APC is a strongly predisposing event in the development of colorectal cancer, prompting the search for vulnerabilities specific to cells that have lost APC function. Signalling through the mTOR pathway is known to be required for epithelial cell proliferation and tumour growth, and the current paradigm suggests that a critical function of mTOR activity is to upregulate translational initiation through phosphorylation of 4EBP1 (refs 6, 7). This model predicts that the mTOR inhibitor rapamycin, which does not efficiently inhibit 4EBP1 (ref. 8), would be ineffective in limiting cancer progression in APC-deficient lesions. Here we show in mice that mTOR complex 1 (mTORC1) activity is absolutely required for the proliferation of Apc-deficient (but not wild-type) enterocytes, revealing an unexpected opportunity for therapeutic intervention. Although APC-deficient cells show the expected increases in protein synthesis, our study reveals that it is translation elongation, and not initiation, which is the rate-limiting component. Mechanistically, mTORC1-mediated inhibition of eEF2 kinase is required for the proliferation of APC-deficient cells. Importantly, treatment of established APC-deficient adenomas with rapamycin (which can target eEF2 through the mTORC1-S6K-eEF2K axis) causes tumour cells to undergo growth arrest and differentiation. Taken together, our data suggest that inhibition of translation elongation using existing, clinically approved drugs, such as the rapalogs, would provide clear therapeutic benefit for patients at high risk of developing colorectal cancer