A systematic review of language and literacy interventions in children and adolescents with English as an additional language (EAL)

This systematic review presents a synthesis of evidence regarding the effectiveness of language and literacy interventions targeting children with EAL. It updates the systematic review by Murphy and Unthiah [2015. A systematic review of intervention research examining English language and literacy development in children with English as an additional language (EAL). http://www.naldic.org.uk/Resources/NALDIC/Research and Information/Documents/eal-systematic-review-prof-v-murphy.pdf.], using the same methodology. Four databases were searched resulting in 2217 records identified. After screening 25 interventions, found in 26 studies, were eligible for inclusion. The results provide collective evidence that explicit vocabulary instruction and targeted oral language practice yield language gains for EAL learners, with a tendency for larger intervention gains in learners with the lowest initial pre-test scores. Shared reading interventions show positive effects when combined with the pre-teaching of vocabulary, embedded definitions into the text, or post-reading reinforcement activities. The review also highlights the paucity of interventions in the UK and in particular, a lack of interventions for adolescents, especially those in upper secondary school (ages 14-18)

Examining the Relationship between Traumatic Experiences and Posttraumatic Growth among Counselors-in-Training

The present study explored the relationship between experience of trauma and posttraumatic growth (PTG) among 86 graduate level counselors-in-training (CIT). Results indicated that the most frequent trauma endorsed was witnessed or learned about violence to a loved one and the higher the rating of the most severe trauma experienced related to a higher reported level of personal growth. Overall, 67% of the CIT received support for their trauma by participating in personal counseling. Implications for counselor educators includes an understanding of the potential for trauma impacting students as well as different responses to trauma based on gender and the number of traumatic experiences

Health-related quality of life among Ebola survivors in Sierra Leone: the role of socio-demographic, health-related and psycho-social factors.

BACKGROUND: Evidence of how social factors affect the health-related quality of life (HRQoL) of Ebola virus disease (EVD) survivors is limited. Our study explores the association between socio-demographic, health-related and psycho-social (stigma) factors and EVD survivors' health-related quality of life (HRQoL) in Sierra Leone. METHODS: We conducted a nationwide cross-sectional study among 358 EVD survivors between January and August 2018. We used a multistage sampling method to recruit EVD survivors, and the RAND 36-Item Health Survey item was used to assess the HRQoL. Data were analysed using descriptive statistics and multiple linear regression. RESULTS: When comparing by each dimension in relation to their respective summary scores, role limitation physical [0.00 (50.00)] and role limitation emotional [0.00 (33.33)] were the most affected physical health and mental health domains among EVD survivors respectively. EVD survivors who were older (β = - 3.90, 95% CI - 6.47 to - 1.32, p = 0.003), had no formal education (β = - 2.80, 95% CI - 5.16 to - 0.43, p = 0.021), experienced a unit increase in the number of post-Ebola symptoms (β = - 1.08, 95% CI - 1.74 to - 0.43, p < 0.001) and experienced a unit increase in enacted stigma (β = - 2.61, 95% CI - 4.02 to - 1.20, p < 0.001) were more likely to report a decreased level of physical health. EVD survivors who experienced a unit increase in the time spent in the Ebola treatment centre (β = - 0.60, 95% CI - 0.103 to - 0.18, p = 0.006) and those who experienced a unit increase in enacted Stigma were more likely to report decreased levels of mental health (β = - 1.50, 95% CI - 2.67 to - 0.33, p = 0.012). CONCLUSION: Sociodemographic, health-related, and psycho-social factors were significantly associated with decrease levels of HRQoL. Our findings improve our understanding of the factors that might influence the HRQoL and suggest the need for EVD survivors to be provided with a comprehensive healthcare package that caters for their physical and mental health needs

CARDIOVASCULAR AND HEMODYNAMIC EFFECTS OF GLUCAGON-LIKE PEPTIDE-1

Glucagon-like peptide-1 (GLP-1) is an incretin hormone that has been shown to have hemodynamic and cardioprotective capacity in addition to its better characterized glucoregulatory actions. Because of this, emerging research has focused on the ability of GLP-1 based therapies to drive myocardial substrate selection, enhance cardiac performance and regulate heart rate, blood pressure and vascular tone. These studies have produced consistent and reproducible results amongst numerous laboratories. However, there are obvious disparities in findings obtained in small animal models versus those of higher mammals. This species dependent discrepancy calls to question, the translational value of individual findings. Moreover, few studies of GLP-1 mediated cardiovascular action have been performed in the presence of a pre-existing comorbidities (e.g. obesity/diabetes) which limits interpretation of the effectiveness of incretin-based therapies in the setting of disease. This review addresses cardiovascular and hemodynamic potential of GLP-1 based therapies with attention to species specific effects as well as the interaction between therapies and disease

Cost-effectiveness analysis of introducing RDTs for malaria diagnosis as compared to microscopy and presumptive diagnosis in central and peripheral public health facilities in Ghana.

Cost-effectiveness information on where malaria rapid diagnostic tests (RDTs) should be introduced is limited. We developed incremental cost-effectiveness analyses with data from rural health facilities in Ghana with and without microscopy. In the latter, where diagnosis had been presumptive, the introduction of RDTs increased the proportion of patients who were correctly treated in relation to treatment with antimalarials, from 42% to 65% at an incremental societal cost of Ghana cedis (GHS)12.2 (US$8.3) per additional correctly treated patients. In the "microscopy setting" there was no advantage to replacing microscopy by RDT as the cost and proportion of correctly treated patients were similar. Results were sensitive to a decrease in the cost of RDTs, which cost GHS1.72 (US$1.17) per test at the time of the study and to improvements in adherence to negative tests that was just above 50% for both RDTs and microscopy

Perivascular adipose tissue and coronary vascular disease

Coronary perivascular adipose tissue is a naturally occurring adipose tissue depot that normally surrounds the major coronary arteries on the surface of the heart. Although originally thought to promote vascular health and integrity, there is a growing body of evidence to support that coronary perivascular adipose tissue displays a distinct phenotype relative to other adipose depots and is capable of producing local factors with the potential to augment coronary vascular tone, inflammation, and the initiation and progression of coronary artery disease. The purpose of the present review is to outline previous findings about the cardiovascular effects of coronary perivascular adipose tissue and the potential mechanisms by which adipose-derived factors may influence coronary vascular function and the progression of atherogenesis

First report of Rice stripe necrosis virus infecting rice in Sierra Leone

While Rice stripe necrosis virus (RSNV, Benyvirus, Benyviridae) has been reported on rice plants on two continents, little is known about the diversity of this multipartite virus which is transmitted by the plasmodiophorid protist Polymyxa graminis. First identified in 1983 in the Côte d´Ivoire (Fauquet & Thouvenel, 1983), the disease had previously been observed in Sierra Leone without formal identification of the causal agent (Buddenhagen, pers. comm.). Later, the virus was reported in South and Central America (Colombia, Ecuador, Panama and Brazil) causing up to 40% yield losses (Morales et al., 1999). Recently, RSNV was identified for the first time in several African countries including Burkina Faso (Sérémé et al., 2014), Benin (Oludare et al., 2015) and Mali (Decroës et al., 2017) suggesting a re-emergence of the virus in Africa.In 2019, symptoms of leaf-crinkling and stripe necrosis were observed on a rice plant from the Bo District in Sierra Leone (Fig. 1). Leaf samples were analysed by serological and molecular methods to confirm the presence of RSNV in Sierra Leone. RSNV was detected by plate-trapped antibody (PTA)- ELISA using a polyclonal antiserum against RSNV (Fauquet & Thouvenel, 1983).The presence of the virus was confirmed after total RNA extraction using 0.05 g of leaves and the RNeasy Plant Mini Kit (Qiagen) and RT-PCR amplification (10 U/μl M-MLV-reverse transcriptase, Promega; 10 U/μl Dynazyme, Finnzyme) as described previously (Sérémé et al., 2014, Oludare et al., 2015) with primers RSNV1-2901F 5′-TGAATTTGGTGCTCTCTTG-3′ / RSNV1-3827R 5′-TGTGGCGTTTCCAGACCTAAA-3´ and RSNV2-5´ 5´-TATCACTACTGACGAATTCCACCTAC-3´ / RSNV2-1223R 5´-AATCTGCGGCCTGTTTTGTA-3´. Specific amplicons, 926 and 1241 nt in length, were generated corresponding to sequences in the helicase domain and the coat protein (CP) genes on RSNV RNA 1 and RNA 2, respectively. The amplicons were sequenced directly and the sequences deposited in GenBank (Accession Nos. MN750254 and MN750255, respectively).The helicase sequence obtained from the Sierra Leone RSNV isolate showed 1.8-7.3% genetic distance with those from South America (EU099844.3, MG792544, MG792545, MG792546) and only 1.4-2.2% with those from Africa (KP099623, MF115599, MF115600, MF115601, MF115602, MF115603, MK170452, MK170453). The phylogenetic analysis based on the helicase domain included the sequence obtained from the Sierra Leone within a cluster represented by RSNV from South America and West Africa (Fig. 2a). In contrast, the CP sequence from the Sierra Leone RSNV isolate revealed an unexpected genetic differentiation as compared to all the other sequences from South America (5.6%; NC_038774) or Africa (5.2-6.5%; LK023710, MF115604, MF115605, MF115606, MF115607, MF115608, MK170454, MK170455). Interestingly, the CP sequence from Sierra Leone is located at a basal position in the phylogeny (Fig. 2b).To our knowledge, this is the first confirmed report of RSNV in Sierra Leone. Further studies are needed to assess the molecular and biological diversity of RSNV, the spatial distribution and the incidence of this re-emerging rice disease in Africa.Fil: Tucker, M. J.. Sierra Leone Agricultural Research Institute; Sierra LeonaFil: Giovani Celli, Marcos Giovani. Instituto Nacional de Tecnología Agropecuaria. Centro de Investigaciones Agropecuarias. Unidad de Fitopatología y Modelización Agrícola - Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Unidad de Fitopatología y Modelización Agrícola; ArgentinaFil: Conteh, A. B.. Sierra Leone Agricultural Research Institute; Sierra LeonaFil: Taylor, D. R.. Sierra Leone Agricultural Research Institute; Sierra LeonaFil: Hebrard, Andrés. Centre National de la Recherche Scientifique. Institut de Recherche pour le Développement; FranciaFil: Poulicard, N.. Centre National de la Recherche Scientifique. Institut de Recherche pour le Développement; Franci

Pancreatic beta cell autophagy is impaired in type 1 diabetes

Aims/hypothesis Pancreatic beta cells are subjected to exogenous damaging factors such as proinflammatory cytokines or excess glucose that can cause accumulation of damage-inducing reactive oxygen species during the pathogenesis of diabetes. We and others have shown that beta cell autophagy can reduce reactive oxygen species to protect against apoptosis. While impaired islet autophagy has been demonstrated in human type 2 diabetes, it is unknown if islet autophagy is perturbed in the pathogenesis of type 1 diabetes. We hypothesised that beta cell autophagy is dysfunctional in type 1 diabetes, and that there is a progressive loss during early diabetes development. Methods Pancreases were collected from chloroquine-injected and non-injected non-obese diabetes-resistant (NOR) and non-obese diabetic (NOD) mice. Age- and BMI-matched pancreas tissue sections from human organ donors (N = 34) were obtained from the Network for Pancreatic Organ Donors with Diabetes (nPOD). Tissue sections were stained with antibodies against proinsulin or insulin (beta cell markers), microtubule-associated protein 1 light chain 3 A/B (LC3A/B; autophagosome marker), lysosomal-associated membrane protein 1 (LAMP1; lysosome marker) and p62 (autophagy adaptor). Images collected on a scanning laser confocal microscope were analysed with CellProfiler and ImageJ. Secondary lysosomes and telolysosomes were assessed in electron micrographs of human pancreatic tissue sections (n = 12), and energy dispersive x-ray analysis was performed to assess distribution of elements (n = 5). Results We observed increased autophagosome numbers in islets of diabetic NOD mice (p = 0.008) and increased p62 in islets of both non-diabetic and diabetic NOD mice (p < 0.001) vs NOR mice. There was also a reduction in LC3-LAMP1 colocalisation in islets of diabetic NOD mice compared with both non-diabetic NOD (p < 0.001) and NOR mice (p < 0.001). Chloroquine elicited accumulation of autophagosomes in the islets of NOR (p = 0.003) and non-diabetic NOD mice (p < 0.001), but not in islets of diabetic NOD mice; and stimulated accumulation of p62 in NOR (p < 0.001), but not in NOD mice. We observed reduced LC3-LAMP1 colocalisation (p < 0.001) in residual beta cells of human donors with type 1 diabetes vs non-diabetic participants. We also observed reduced colocalisation of proinsulin with LAMP1 in donors with type 1 diabetes (p < 0.001). Electron microscopy also revealed accumulation of telolysosomes with nitrogen-dense rings in beta cells of autoantibody-positive donors (p = 0.002). Conclusions/interpretation We provide evidence of islet macroautophagy/crinophagy impairment in human type 1 diabetes. We also document accumulation of telolysosomes with peripheral nitrogen in beta cells of autoantibody-positive donors, demonstrating altered lysosome content that may be associated with lysosome dysfunction before clinical hyperglycaemia. Similar macroautophagy impairments are present in the NOD mouse model of type 1 diabetes

Obesity Alters Molecular and Functional Cardiac Responses to Ischemia-Reperfusion and Glucagon-Like Peptide-1 Receptor Agonism

This study tested the hypothesis that obesity alters the cardiac response to ischemia/reperfusion and/or glucagon like peptide-1 (GLP-1) receptor activation, and that these differences are associated with alterations in the obese cardiac proteome and microRNA (miRNA) transcriptome. Ossabaw swine were fed normal chow or obesogenic diet for 6 months. Cardiac function was assessed at baseline, during a 30-minutes coronary occlusion, and during 2 hours of reperfusion in anesthetized swine treated with saline or exendin-4 for 24 hours. Cardiac biopsies were obtained from normal and ischemia/reperfusion territories. Fat-fed animals were heavier, and exhibited hyperinsulinemia, hyperglycemia, and hypertriglyceridemia. Plasma troponin-I concentration (index of myocardial injury) was increased following ischemia/reperfusion and decreased by exendin-4 treatment in both groups. Ischemia/reperfusion produced reductions in systolic pressure and stroke volume in lean swine. These indices were higher in obese hearts at baseline and relatively maintained throughout ischemia/reperfusion. Exendin-4 administration increased systolic pressure in lean swine but did not affect the blood pressure in obese swine. End-diastolic volume was reduced by exendin-4 following ischemia/reperfusion in obese swine. These divergent physiologic responses were associated with obesity-related differences in proteins related to myocardial structure/function (e.g. titin) and calcium handling (e.g. SERCA2a, histidine-rich Ca2+ binding protein). Alterations in expression of cardiac miRs in obese hearts included miR-15, miR-27, miR-130, miR-181, and let-7. Taken together, these observations validate this discovery approach and reveal novel associations that suggest previously undiscovered mechanisms contributing to the effects of obesity on the heart and contributing to the actions of GLP-1 following ischemia/reperfusion

Glucagon-like peptide-1 (7-36) but not (9-36) augments cardiac output during myocardial ischemia via a Frank-Starling mechanism

This study examined the cardiovascular effects of GLP-1 (7-36) or (9-36) on myocardial oxygen consumption, function and systemic hemodynamics in vivo during normal perfusion and during acute, regional myocardial ischemia. Lean Ossabaw swine received systemic infusions of saline vehicle or GLP-1 (7-36 or 9-36) at 1.5, 3.0, and 10.0 pmol/kg/min in sequence for 30 min at each dose, followed by ligation of the left circumflex artery during continued infusion at 10.0 pmol/kg/min. Systemic GLP-1 (9-36) had no effect on coronary flow, blood pressure, heart rate or indices of cardiac function before or during regional myocardial ischemia. Systemic GLP-1 (7-36) exerted no cardiometabolic or hemodynamic effects prior to ischemia. During ischemia, GLP-1 (7-36) increased cardiac output by approximately 2 L/min relative to vehicle-controls (p = 0.003). This response was not diminished by treatment with the non-depolarizing ganglionic blocker hexamethonium. Left ventricular pressure-volume loops measured during steady-state conditions with graded occlusion of the inferior vena cava to assess load-independent contractility revealed that GLP-1 (7-36) produced marked increases in end-diastolic volume (74 ± 1 to 92 ± 5 ml; p = 0.03) and volume axis intercept (8 ± 2 to 26 ± 8; p = 0.05), without any change in the slope of the end-systolic pressure-volume relationship vs. vehicle during regional ischemia. GLP-1 (9-36) produced no changes in any of these parameters compared to vehicle. These findings indicate that short-term systemic treatment with GLP-1 (7-36) but not GLP-1 (9-36) significantly augments cardiac output during regional myocardial ischemia, via increases in ventricular preload without changes in cardiac inotropy