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This research sought to investigate EFL nursing students' use of vocabulary learning strategies to learn medical terminology and further assess strategies used in relation to learning outcomes measured by two types of vocabulary knowledge: meaning recall (passive recall) and meaning recognition (passive recognition). The participants, 138 EFL nursing students in Taiwan, completed a meaning recall test and a meaning recognition test in week 8 of the semester, and they then took the English proficiency test (TOEIC Bridge) and filled out a vocabulary learning strategies survey in the following week. Both vocabulary outcomes had moderate correlations with English proficiency. Strategy use patterns appeared for the nursing students' medical terminology acquisition. They focused on looking up for corresponding meaning in L1 using a search engine, then learning orthographical and phonological forms to facilitate retention. A Pearson Correlation Analysis revealed that inferring word meaning, utilizing mnemonic devices for retention, and managing vocabulary learning were significantly and positively correlated with both vocabulary scores. In contrast, social strategies were the least conducive to achievement.

Though there are a multiplicity of approaches that have been used to promote Nature of Science (NOS) among school students, an approach based on exploration of a scientific discovery indigenous to the sample population, of contemporary interest, and based on a topic outside the school science syllabus seems to be lacking in the literature. This study focused on Chinese high school students (N = 98), using the discovery of an anti-malarial drug by a recent Nobel Prize winning Chinese scientist as a focus. A popular science article on this discovery formed the basis for the intervention, and a mainly qualitative approach was used. Variants of an explicit-reflective approach were used for the three groups formed by random sampling for the intervention. The four NOS attributes targeted were: socio-cultural, empirical nature, scientific method, and creativity/imagination, and these were explicitly interrogated through four open-ended questions, respectively. Responses to these questions were parked into five rating levels, which helped to explicate the extent to which the samples were able to provide descriptors to characterize their understandings. The approach based on reading of the article followed by student discussions and mediation by the instructor showed, overall, more gains in NOS as compared to just: (1) reading/re-reading of the article and reflecting on it; and (2) reading of the article followed by small sub-group discussions and reflecting on it. It is suggested that there is a case for using indigenous scientific discovery as an approach to foster interest in NOS among students. Some implications of the study are discussed.

During the last 40 years, neuroscience has become one of the most central and most productive approaches to investigating autism. In this commentary, we assemble a group of established investigators and trainees to review key advances and anticipated developments in neuroscience research across five modalities most commonly employed in autism research: magnetic resonance imaging, functional near infrared spectroscopy, positron emission tomography, electroencephalography, and transcranial magnetic stimulation. Broadly, neuroscience research has provided important insights into brain systems involved in autism but not yet mechanistic understanding. Methodological advancements are expected to proffer deeper understanding of neural circuitry associated with function and dysfunction during the next 40 years.

Abstract Background The American College of Medical Genetics and Genomics (ACMG)/Association for Molecular Pathology (AMP) guidelines recommend using variant enrichment among cases as "strong" evidence for pathogenicity per the PS4 criterion. However, quantitative support for PS4 thresholds from real-world Mendelian case–control cohorts is lacking. Methods To address this gap, we evaluated and established PS4 thresholds using data from the Chinese Deafness Genetics Consortium. A total of 9,050 variants from 13,845 patients with hearing loss (HL) and 6,570 ancestry-matched controls were analyzed. Positive likelihood ratio and local positive likelihood ratio values were calculated to determine the thresholds corresponding to each strength of evidence across three variant subsets. Results In subset 1, consisting of variants present in both cases and controls with an allele frequency (AF) in cases ≥ 0.0005, an odds ratio (OR) ≥ 6 achieved strong evidence, while OR ≥ 3 represented moderate evidence. For subset 2, which encompassed variants present in both cases and controls with a case AF 2.27 or allele count ≥ 3) and the PS4_Moderate threshold (allele count ≥ 6), respectively. Reanalysis applying the adjusted PS4 criteria changed the classification of 15 variants and enabled diagnosis of an additional four patients. Conclusions Our study quantified evidence strength thresholds for variant enrichment in genetic HL cases, highlighting the importance of defining disease/gene-specific thresholds to improve the precision and accuracy of clinical genetic testing.

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Copyright of Cadernos de Saude Publica is the property of Escola Nacional de Saude Publica Sergio Arouca and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The yearly increase in government R&D investment and top-down national R&D investment allocation requires a more quantitative decision-making system that maximizes R&D performance and efficient budget allocation. Sound decision-making is necessary at both the selection stage and the pursuit stage in order to maximize limited national R&D resources. We study Korean smart farms as an example to examine national R&D investment from the various R&D actors (academia, industry, and research institutes) perspectives. The objective of our research is to evaluate the theoretical efficiency of R&D investment on specific technologies in smart farms and compare the results with expert opinions where the reality is reflected. To be specific, our study is to provide the quantitative approach in making decision among policymakers by reflecting the field experiences and opinions. We use a data envelopment analysis with an assurance region model, which integrates an analytic hierarchy process and a data envelopment analysis. The weights of output in DEA model by the R&D actors are similar to the overall weight by all actors, implying that investment allocation decisions in the smart farm sector are not significantly affected by the R&D actors. We realized that the relative efficiency of some R&D technologies increases after reflecting qualitative ideas of experts. In reality, it is necessary to invest in these technology groups, but they excluded from top-down decision-making. This also shows that a government’s top-down decision-making can distort its investment allocation. This study proposes a new approach to compensate for the difference between theoretical virtual prices and actual prices in data envelopment analysis. In particular, when comparing the only quantitative results on investment priorities with analysis results by additionally reflecting the opinions of experts in each sector, we found that the Korean government’s investment priorities in the smart farm field are considerably distorted. Therefore, this study is expected to be used as an alternative for policy makers to compensate for the quantitative distortion might be caused by top-down national R&D investment decisions.

Atrial septal defect (ASD) is one of the most common congenital heart defects diagnosed in children. Sarcomeric genes has been attributed to ASD and knockdown of MYH3 functionally homologues gene in chick models indicated abnormal atrial septal development. Here, we report for the first time, a case-control study investigating the role of MYH3 among non-syndromic ASD patients in contributing to septal development. Four amplicons which will amplifies the 40 kb MYH3 were designed and amplified using long range-PCR. The amplicons were then sequenced using indexed paired-end libraries on the MiSeq platform. The STREGA guidelines were applied for planning and reporting. The non-synonymous c. 3574G>A (p.Ala1192Thr) [p = 0.001, OR = 2.30 (1.36-3.87)] located within the tail domain indicated a highly conserved protein region. The mutant model of c. 3574G>A (p.Ala1192Thr) showed high root mean square deviation (RMSD) values compared to the wild model. To our knowledge, this is the first study to provide compelling evidence on the pathogenesis of MYH3 variants towards ASD hence, suggesting the crucial role of non-synonymous variants in the tail domain of MYH3 towards atrial septal development. It is hoped that this gene can be used as panel for diagnosis of ASD in future.

Aim/Hypothesis The adult mammalian pancreas has limited ability to regenerate in order to restore adequate insulin production from multipotent progenitors, the identity and function of which remain poorly understood. Here we test whether the TNF family member TWEAK (TNF-like weak inducer of apoptosis) promotes β-cell neogenesis from proliferating pancreatic ductal epithelium in adult mice. Methods: C57Bl/6J mice were treated with Fc-TWEAK and pancreas harvested at different time points for analysis by histology and immunohistochemistry. For lineage tracing, 4 week old double transgenic mice CAII-CreERTM: R26R-eYFP were implanted with tamoxifen pellet, injected with Fc-TWEAK or control Ig twice weekly and analyzed at day 18 for TWEAK-induced duct cell progeny by costaining for insulin and YFP. The effect of TWEAK on pancreatic regeneration was determined by pancytokeratin immunostaining of paraffin embedded sections from wildtype and TWEAK receptor (Fn14) deficient mice after Px. Results: TWEAK stimulates proliferation of ductal epithelial cells through its receptor Fn14, while it has no mitogenic effect on pancreatic α- or β-cells or acinar cells. Importantly, TWEAK induces transient expression of endogenous Ngn3, a master regulator of endocrine cell development, and induces focal ductal structures with characteristics of regeneration foci. In addition, we identify by lineage tracing TWEAK-induced pancreatic β-cells derived from pancreatic duct epithelial cells. Conversely, we show that Fn14 deficiency delays formation of regenerating foci after Px and limits their expansion. Conclusions/Interpretation We conclude that TWEAK is a novel factor mediating pancreatic β-cell neogenesis from ductal epithelium in normal adult mice.

Background: Mild retinopathy (microaneurysms or dot-blot hemorrhages) is observed in persons without diabetes or hypertension and may reflect microvascular disease in other organs. We conducted a genome-wide association study (GWAS) of mild retinopathy in persons without diabetes. Methods: A working group agreed on phenotype harmonization, covariate selection and analytic plans for within-cohort GWAS. An inverse-variance weighted fixed effects meta-analysis was performed with GWAS results from six cohorts of 19,411 Caucasians. The primary analysis included individuals without diabetes and secondary analyses were stratified by hypertension status. We also singled out the results from single nucleotide polymorphisms (SNPs) previously shown to be associated with diabetes and hypertension, the two most common causes of retinopathy. Results: No SNPs reached genome-wide significance in the primary analysis or the secondary analysis of participants with hypertension. SNP, rs12155400, in the histone deacetylase 9 gene (HDAC9) on chromosome 7, was associated with retinopathy in analysis of participants without hypertension, −1.3±0.23 (beta ± standard error), \(p = 6.6×10^{-9}\). Evidence suggests this was a false positive finding. The minor allele frequency was low (∼2%), the quality of the imputation was moderate \((r^{2} ∼0.7)\), and no other common variants in the HDAC9 gene were associated with the outcome. SNPs found to be associated with diabetes and hypertension in other GWAS were not associated with retinopathy in persons without diabetes or in subgroups with or without hypertension. Conclusions: This GWAS of retinopathy in individuals without diabetes showed little evidence of genetic associations. Further studies are needed to identify genes associated with these signs in order to help unravel novel pathways and determinants of microvascular diseases.

Recent studies have shown that a tumor-supportive microenvironment is characterized by high levels of pro-inflammatory and pro-angiogenic eicosanoids derived from omega-6 (n−6) arachidonic acid (AA). Although the metabolic pathways (COX, LOX, and P450) that generate these n−6 AA eicosanoids have been targeted, the role of endogenous AA production in tumorigenesis remains unexplored. Delta-6 desaturase (D6D) is the rate-limiting enzyme responsible for the synthesis of n−6 AA and increased D6D activity can lead to enhanced n−6 AA production. Here, we show that D6D activity is upregulated during melanoma and lung tumor growth and that suppressing D6D activity, either by RNAi knockdown or a specific D6D inhibitor, dramatically reduces tumor growth. Accordingly, the content of AA and AA-derived tumor-promoting metabolites is significantly decreased. Angiogenesis and inflammatory status are also reduced. These results identify D6D as a key factor for tumor growth and as a potential target for cancer therapy and prevention.

Recent evidence suggests that the observed clinical distinctions between lung tumors in smokers and never smokers (NS) extend beyond specific gene mutations, such as EGFR, EML4-ALK, and KRAS, some of which have been translated into targeted therapies. However, the molecular alterations identified thus far cannot explain all of the clinical and biological disparities observed in lung tumors of NS and smokers. To this end, we performed an unbiased genome-wide, comparative study to identify novel genomic aberrations that differ between smokers and NS. High resolution whole genome DNA copy number profiling of 69 lung adenocarcinomas from smokers (n = 39) and NS (n = 30) revealed both global and regional disparities in the tumor genomes of these two groups. We found that NS lung tumors had a greater proportion of their genomes altered than those of smokers. Moreover, copy number gains on chromosomes 5q, 7p, and 16p occurred more frequently in NS. We validated our findings in two independently generated public datasets. Our findings provide a novel line of evidence distinguishing genetic differences between smoker and NS lung tumors, namely, that the extent of segmental genomic alterations is greater in NS tumors. Collectively, our findings provide evidence that these lung tumors are globally and genetically different, which implies they are likely driven by distinct molecular mechanisms.

Objective: To explore common reasons for non-adherence to treatment in patients with rheumatoid arthritis in Singapore. Methods: Patients diagnosed with rheumatoid arthritis for ⩾ 1 year being followed up at the Singapore General Hospital and meeting pre-defined criteria of non-adherence were invited to participate in focus groups to discuss issues related to adherence to their rheumatoid arthritis treatment. Each focus group was homogenous in terms of gender, language spoken and ethnicity. Discussions were audio recorded and subsequently transcribed verbatim for thematic analysis. Results: Of the 26 patients who participated in the study, seven reported non-adherence to medication, two reported non-adherence to doctors’ appointments, and 11 reported non-adherence to both. The most commonly mentioned reasons for non-adherence were forgetfulness ( n =13), low perceived need for treatment ( n =10), actual or perceived medication side effects ( n =6) and intentional delay due to busyness ( n =4). Eleven participants acknowledged more than one of these four reasons for non-adherence. Conclusion: There are multiple reasons for non-adherence to treatment among patients with rheumatoid arthritis in Singapore. Findings from this study provide important empirical evidence to inform strategies to improve adherence and in turn treatment outcomes for this group of patients in Singapore.

MicroRNAs are endogenous, small non-coding RNAs approximately 18-26 nucleotides in length that regulate target gene expression at the post-transcription level. Interferon-γ (IFN-γ) is a Th1 cytokine that is involved in both the innate and adaptive immune responses. We previously identified two IFN-γ genes in green-spotted puffer fish (Tetraodon nigroviridis). To determine whether miRNAs participate in IFN-γ-related immune responses, T. nigroviridis spleen cells were treated with recombinant IFN-γ isoforms, and a Solexa high-throughput sequencing method was used to identify miRNAs. In total, 1,556, 1,538 and 1,573 miRNAs were found in the three samples, and differentially expressed miRNAs were determined. In total, 398 miRNAs were differentially expressed after rIFN-γ1 treatment, and 438 miRNAs were differentially expressed after rIFN-γ2 treatment; additionally, 403 miRNAs were differentially expressed between the treatment groups. Ten differentially expressed miRNAs were chosen for validation using qRT-PCR. Target genes for the differentially expressed miRNAs were predicted, and GO and KEGG analyses were performed. This study provides basic knowledge regarding fish IFN-γ-induced miRNAs and offers clues for further studies into the mechanisms underlying fish IFN-γ-mediated immune responses.