Working on Literacy in CLIL/Bilingual Contexts: Reading to Learn and Teacher Development

This paper describes a project implementing a literacy programme based on a linguistic approach to teaching reading and writing, found especially useful for subject classes taught through a foreign language. The programme, Reading to Learn (Rose, 2014; Rose & Martin, 2012), based on an analysis of the genres of different subjects, their language features and the diffi culties these pose learners, offers teachers an explicit and detailed method to approach text comprehension/production. The paper includes examples of texts from late primary to mid-secondary content classes as analysed and used by teachers, student texts, and reactions to the pedagogy.Este trabajo presenta un programa de formación para la enseñanza de la lengua escrita en las diferentes áreas curriculares, implementado en las clases de contenido impartidas en una lengua extranjera. El programa, Leer para Aprender (Rose, 2014; Rose & Martin, 2012), se fundamenta en el análisis de los géneros de las disciplinas escolares, sus rasgos lingüísticos, y dificultades para los aprendices, y ofrece al docente una secuencia didáctica explícita y detallada con la que enfrentarse a la comprensión y producción de textos. Se incluyen ejemplos del trabajo de los profesores (análisis, diseño de la interacción) y de producción escrita de alumnos, así como la evaluación del proyecto

Osteocyte dysfunction promotes osteoarthritis through MMP13-dependent suppression of subchondral bone homeostasis.

Osteoarthritis (OA), long considered a primary disorder of articular cartilage, is commonly associated with subchondral bone sclerosis. However, the cellular mechanisms responsible for changes to subchondral bone in OA, and the extent to which these changes are drivers of or a secondary reaction to cartilage degeneration, remain unclear. In knee joints from human patients with end-stage OA, we found evidence of profound defects in osteocyte function. Suppression of osteocyte perilacunar/canalicular remodeling (PLR) was most severe in the medial compartment of OA subchondral bone, with lower protease expression, diminished canalicular networks, and disorganized and hypermineralized extracellular matrix. As a step toward evaluating the causality of PLR suppression in OA, we ablated the PLR enzyme MMP13 in osteocytes while leaving chondrocytic MMP13 intact, using Cre recombinase driven by the 9.6-kb DMP1 promoter. Not only did osteocytic MMP13 deficiency suppress PLR in cortical and subchondral bone, but it also compromised cartilage. Even in the absence of injury, osteocytic MMP13 deficiency was sufficient to reduce cartilage proteoglycan content, change chondrocyte production of collagen II, aggrecan, and MMP13, and increase the incidence of cartilage lesions, consistent with early OA. Thus, in humans and mice, defects in PLR coincide with cartilage defects. Osteocyte-derived MMP13 emerges as a critical regulator of cartilage homeostasis, likely via its effects on PLR. Together, these findings implicate osteocytes in bone-cartilage crosstalk in the joint and suggest a causal role for suppressed perilacunar/canalicular remodeling in osteoarthritis

Improving Fatigue Evaluations of Structures Using In-Service Behavior Measurement Data

Conservative models and code practices are usually employed for fatigue-damage predictions of existing structures. Direct in-service behavior measurements are able to provide more accurate estimations of remaining-fatigue-life predictions. However, these estimations are often accurate only for measured locations and measured load conditions. Behavior models are necessary for exploiting information given by measurements and predicting the fatigue damage at all critical locations and for other load cases. Model-prediction accuracy can be improved using system identification techniques where the properties of structures are inferred using behavior measurements. Building upon recent developments in system identification where both model and measurement uncertainties are considered, this paper presents a new data-interpretation framework for reducing uncertainties related to prediction of fatigue life. An initial experimental investigation confirms that, compared with traditional engineering approaches, the methodology provides a safe and more realistic estimation of the fatigue reserve capacity. A second application on a full-scale bridge also confirms that using load-test data reduces the uncertainty related to remaining-fatigue-life predictions

Measurement, Data Interpretation, and Uncertainty Propagation for Fatigue Assessments of Structures

Real behavior of existing structures is usually associated with large uncertainty that is often covered by the use of conservative models and code practices for the evaluation of remaining fatigue lives. In order to make better decisions related to retrofit and replacement of existing bridges, new techniques that are able to quantify fatigue reserve capacity are required. This paper presents a population-based prognosis methodology that takes advantage of in-service behavior measurements using model-based data interpretation. This approach is combined with advanced traffic and fatigue models to refine remaining-fatigue-life predictions. The study of a full-scale bridge demonstrates that this methodology provides less conservative estimations of remaining fatigue lives. In addition, this approach propagates uncertainties associated with finite-element, traffic and fatigue-damage models to quantify their effects on fatigue-damage assessments and shows that traffic models and structural model parameters are the most influential sources of uncertainty

Reprogramming within Hours Following Nuclear Transfer into Mouse but not Human Zygotes

Fertilized mouse zygotes can reprogram somatic cells to a pluripotent state. Human zygotes might therefore be useful for producing patient-derived pluripotent stem cells. However, logistical, legal and social considerations have limited the availability of human eggs for research. Here we show that a significant number of normal fertilized eggs (zygotes) can be obtained for reprogramming studies. Using these zygotes, we found that when the zygotic genome was replaced with that of a somatic cell, development progressed normally throughout the cleavage stages, but then arrested before the morula stage. This arrest was associated with a failure to activate transcription in the transferred somatic genome. In contrast to human zygotes, mouse zygotes reprogrammed the somatic cell genome to a pluripotent state within hours after transfer. Our results suggest that there may be a previously unappreciated barrier to successful human nuclear transfer, and that future studies could focus on the requirements for genome activation.Stem Cell and Regenerative Biolog

Response to comment on 'Amphibian fungal panzootic causes catastrophic and ongoing loss of biodiversity'

Lambert et al. question our retrospective and holistic epidemiological assessment of the role of chytridiomycosis in amphibian declines. Their alternative assessment is narrow and provides an incomplete evaluation of evidence. Adopting this approach limits understanding of infectious disease impacts and hampers conservation efforts. We reaffirm that our study provides unambiguous evidence that chytridiomycosis has affected at least 501 amphibian species

Variability of systemic and oro-dental phenotype in two families with non-lethal Raine syndrome with FAM20C mutations

Background: Raine syndrome (RS) is a rare autosomal recessive bone dysplasia typified by osteosclerosis and dysmorphic facies due to FAM20C mutations. Initially reported as lethal in infancy, survival is possible into adulthood. We describe the molecular analysis and clinical phenotypes of five individuals from two consanguineous Brazilian families with attenuated Raine Syndrome with previously unreported features. Methods: The medical and dental clinical records were reviewed. Extracted deciduous and permanent teeth as well as oral soft tissues were analysed. Whole exome sequencing was undertaken and FAM20C cDNA sequenced in family 1. Results: Family 1 included 3 siblings with hypoplastic Amelogenesis Imperfecta (AI) (inherited abnormal dental enamel formation). Mild facial dysmorphism was noted in the absence of other obvious skeletal or growth abnormalities. A mild hypophosphataemia and soft tissue ectopic mineralization were present. A homozygous FAM20C donor splice site mutation (c.784 + 5 g > c) was identified which led to abnormal cDNA sequence. Family 2 included 2 siblings with hypoplastic AI and tooth dentine abnormalities as part of a more obvious syndrome with facial dysmorphism. There was hypophosphataemia, soft tissue ectopic mineralization, but no osteosclerosis. A homozygous missense mutation in FAM20C (c.1487C > T; p.P496L) was identified. Conclusions: The clinical phenotype of non-lethal Raine Syndrome is more variable, including between affected siblings, than previously described and an adverse impact on bone growth and health may not be a prominent feature. By contrast, a profound failure of dental enamel formation leading to a distinctive hypoplastic AI in all teeth should alert clinicians to the possibility of FAM20C mutations