Moments in transformation: Trainee and newly qualified Lifelong learning teachers’ reconceptualization of assessment in practice

This study investigates the pre-and post-training conceptualisations of assessment amongst trainee and recently qualified teachers in the lifelong learning sector in the UK. Using the lens of transformative learning, the study maps out the process, influential factors and time in the shift in conceptualisation. Though designed as a qualitative iterative study, the study employed a combination of statistical tools and content analysis in data analysis. It found that the dominant pre-training conceptualisation of assessment was in its summative essence as a tool for testing and examination and that reconceptualization occurred mostly during practice. The study calls for a review of the structure and content of teacher education in the area of assessment and proposed that post-training development programmes for newly and recently qualified teachers must acknowledge these findings in their teacher development programmes

Velocity Analysis of Multi-Receiver Full Waveform Acoustic Logging Data In Open and Cased Holes

Average semblance and maximum-likelihood spectral analyses are applied to synthetic and field full waveform acoustic logging data to determine formation velocities. Of particular interest is the ability of these methods to resolve the P and shear/pseudo Rayleigh arrivals in data from poorly-bonded cased boreholes. In synthetic open-hole data the velocity analyses yield results within 4% of the true velocities. Results from synthetic well-bonded cased hole data are generally as good as those from the open hole data. However, if the formation P-wave velocity is within roughly 10% of the plate velocity of the steel pipe (about 5.3-5.5 km/s), then there may be a resonance effect that appears to slow down the P wave slightly (on the order of 6%). For cased-hole models with no steel/cement bonding (the free-pipe situation), the measured P-wave velocities are typically 6 to 8% less than the actual formation velocities. If the formation S-wave velocity is greater than about 2.5 km/s, the S-wave velocity estimate may also be 6 to 8% low. Furthermore, increasing the thickness of either the cement layer or the fluid layer between the pipe and the cement further decreases the formation velocity estimates. Also, if the P-wave velocity is within roughly 15% of the velocity of the steel arrival, the P wave may not be resolved by the semblance method unless the data is first low-pass filtered. Initial tests show that this filtering process may adversely affect the final P-wave velocity estimate, but the details of this type of approach have not been studied. The P wave is resolved. by spectral analysis of the original, unfiltered data. For cased-hole models with no cement/formation bonding (the unbonded-casing situation), formation S-wave velocities are estimated to within 3% relative error, and the formation P-wave velocity is estimated to within 2% error in a slow formation. However, for P-wave velocities between 3.4 km/s and 5.94 km/a, the P wave cannot be resolved by spectral analysis, and it is resolved by the semblance method only in the model with the low velocity (3.4 km/s).Massachusetts Institute of Technology. Full Waveform Acoustic Logging ConsortiumPhillips Petroleum Fellowshi

Update on the Genetics of and Systemic Therapy Options for Combined Hepatocellular Cholangiocarcinoma

Combined hepatocellular-cholangiocarcinoma (cHCC-ICC) is an uncommon and aggressive form of primary liver cancer. Currently, there are no international guidelines for optimal management. For localized tumors, radical resection represents the preferred treatment option, whereas for advanced tumors, systemic therapies recommended for intrahepatic cholangiocarcinoma (ICC) and hepatocellular carcinoma (HCC) are often selected. Emerging information from comparative cohort studies, genomic and transcriptomic data sets are starting to build a case for rationalized approaches to systemic treatment in the advanced setting specific to cHCC-ICC

Hypomanic Defence: Investigating the relationship between depression, response styles and vulnerability to mania

Background: The purpose of this study was to investigate the role of response styles to negative affect in mediating the relationship between depression and vulnerability to experiencing mania. Methods: A cross-sectional correlational design was utilized to examine 217 participants’ responses to an online survey comprising the Hypomanic Personality Scale (HPS), Response Styles Questionnaire (RSQ), and Personal Health Questionaire (PHQ-8). Results: After controlling for covariates (age, gender, ethnicity & depression), rumination, risk-taking and adaptive-coping were all positive predictors of hypomanic personality. Parallel mediation analysis demonstrated that rumination and risk-taking positively mediated the relationship between depression and hypomanic personality, whilst adaptive-coping negatively mediated this relationship. Serial mediation analysis revealed evidence for a sequence of causal mediators, demonstrating that rumination independently predicted risk-taking, which subsequently predicted hypomanic personality. Adaptive-coping continued to supress the relationship between depression and hypomanic personality after including risk-taking in the mediation analysis. Limitations: An unstratified volunteer sampling technique was utilised, introducing potential bias regarding the tendency to adopt maladaptive response styles. Utilising a three-factor response styles solution may lack face validity due to the wide variety of behaviours that encompass adaptive-coping strategies such as pleasant distraction and problem solving. Conclusions: Our findings support the maladaptive role of rumination and risk-taking in mediating the relationship between depression and vulnerability to experience mania, and further substantiates the protective function of adaptive-coping. Clinical interventions may endeavour to diminish the use of rumination and risk-taking, whilst promoting adaptive-coping strategies such as pleasant distraction and problem-solving

Comparison of Bacterial Diversity within the Coral Reef Sponge, Axinella corrugata, and the Encrusting Coral Erythropodium caribaeorum

We compared the Caribbean reef sponge, Axinella corrugata, with the Caribbean reef coral, Erythropodium caribaeorum for differences in their resident microbial communities. This cursory survey of bacterial diversity applied 16S rRNA gene sequences. Over 100 culture-independent sequences were generated from five different Axinella 16S rRNA libraries, and compared with 69 cultured isolates. The cultureindependent 16S rDNA clones displayed a higher diversity of Proteobacteria, including “uncultured” or “unknown” representatives from the Deltaproteobacteria. Arcobacterium, and Cyanobacteria were also found. We have also confirmed that Axinella sponges appeared to host specific microbial symbionts, similar to the previously identified clones termed “OSO” environmental samples. In contrast, seawater samples near Axinella were dominated by Pseudoalteromonas. Adjacent sediment samples yielded clones of Planctomycetacea, Proteobacteria, sulfate-reducing Desulfovibrio spp, and other Deltaproteobacteria. Anaerobe-like 16S rRNA sequences were detected after the oxygen supply to one Axinella sample was deliberately curtailed to assess temporal changes in the microbial community. E. caribaeorum yielded more Betaproteobacteria relative to Axinella 16S libraries, and also included the Gammaproteobacteria genus Spongiobacter. However, Axinella-derived microbes appeared phylogenetically deeper with greater sequence divergences than the coral. Overall this study indicated that marine microbial community diversity can be linked to specific source hosts and habitats

Telomere length and risk of idiopathic pulmonary fibrosis and chronic obstructive pulmonary disease:a mendelian randomisation study

Background: Idiopathic pulmonary fibrosis (IPF) is a fatal lung disease accounting for 1% of UK deaths. In the familial form of pulmonary fibrosis, causal genes have been identified in about 30% of cases, and a majority of these causal genes are associated with telomere maintenance. Prematurely shortened leukocyte telomere length is associated with IPF and chronic obstructive pulmonary disease (COPD), a disease with similar demographics and shared risk factors. Using mendelian randomisation, we investigated evidence supporting a causal role for short telomeres in IPF and COPD. Methods: Mendelian randomisation inference of telomere length causality was done for IPF (up to 1369 cases) and COPD (13 538 cases) against 435 866 controls of European ancestry in UK Biobank. Polygenic risk scores were calculated and two-sample mendelian randomisation analyses were done using seven genetic variants previously associated with telomere length, with replication analysis in an IPF cohort (2668 cases vs 8591 controls) and COPD cohort (15 256 cases vs 47 936 controls). Findings: In the UK Biobank, a genetically instrumented one-SD shorter telomere length was associated with higher odds of IPF (odds ratio [OR] 4·19, 95% CI 2·33–7·55; p=0·0031) but not COPD (1·07, 0·88–1·30; p=0·51). Similarly, an association was found in the IPF replication cohort (12·3, 5·05–30·1; p=0·0015) and not in the COPD replication cohort (1·04, 0·71–1·53; p=0·83). Meta-analysis of the two-sample mendelian randomisation results provided evidence inferring that shorter telomeres cause IPF (5·81 higher odds of IPF, 95% CI 3·56–9·50; p=2·19 × 10−12). There was no evidence to infer that telomere length caused COPD (OR 1·07, 95% CI 0·90–1·27; p=0·46). Interpretation: Cellular senescence is hypothesised as a major driving force in IPF and COPD; telomere shortening might be a contributory factor in IPF, suggesting divergent mechanisms in COPD. Defining a key role for telomere shortening enables greater focus in telomere-related diagnostics, treatments, and the search for a cure in IPF. Investigation of therapies that improve telomere length is warranted. Funding: Medical Research Council.</p

Telomere length and risk of idiopathic pulmonary fibrosis and chronic obstructive pulmonary disease:a mendelian randomisation study

Background: Idiopathic pulmonary fibrosis (IPF) is a fatal lung disease accounting for 1% of UK deaths. In the familial form of pulmonary fibrosis, causal genes have been identified in about 30% of cases, and a majority of these causal genes are associated with telomere maintenance. Prematurely shortened leukocyte telomere length is associated with IPF and chronic obstructive pulmonary disease (COPD), a disease with similar demographics and shared risk factors. Using mendelian randomisation, we investigated evidence supporting a causal role for short telomeres in IPF and COPD. Methods: Mendelian randomisation inference of telomere length causality was done for IPF (up to 1369 cases) and COPD (13 538 cases) against 435 866 controls of European ancestry in UK Biobank. Polygenic risk scores were calculated and two-sample mendelian randomisation analyses were done using seven genetic variants previously associated with telomere length, with replication analysis in an IPF cohort (2668 cases vs 8591 controls) and COPD cohort (15 256 cases vs 47 936 controls). Findings: In the UK Biobank, a genetically instrumented one-SD shorter telomere length was associated with higher odds of IPF (odds ratio [OR] 4·19, 95% CI 2·33–7·55; p=0·0031) but not COPD (1·07, 0·88–1·30; p=0·51). Similarly, an association was found in the IPF replication cohort (12·3, 5·05–30·1; p=0·0015) and not in the COPD replication cohort (1·04, 0·71–1·53; p=0·83). Meta-analysis of the two-sample mendelian randomisation results provided evidence inferring that shorter telomeres cause IPF (5·81 higher odds of IPF, 95% CI 3·56–9·50; p=2·19 × 10−12). There was no evidence to infer that telomere length caused COPD (OR 1·07, 95% CI 0·90–1·27; p=0·46). Interpretation: Cellular senescence is hypothesised as a major driving force in IPF and COPD; telomere shortening might be a contributory factor in IPF, suggesting divergent mechanisms in COPD. Defining a key role for telomere shortening enables greater focus in telomere-related diagnostics, treatments, and the search for a cure in IPF. Investigation of therapies that improve telomere length is warranted. Funding: Medical Research Council.</p