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On February fourteenth, a little girl makes special valentines for everyone she loves--including her puppy who gets a card with a dog biscuit on it.

Scotland is a small country with an education system whose roots lie within an inclusive and egalitarian approach to the education of young people. Subsequent legislation, policies, and curriculum frameworks have been influenced by this, and also by the international move toward equitable, inclusive, and quality lifelong learning for all. Supporting those who are highly able/gifted and talented against such a backdrop offers both opportunities and challenges. In this qualitative study, the Global Principles for Professional Learning in Gifted Education are used to interrogate recent key legislation; the current curriculum framework, Curriculum for Excellence, and the National Framework for Inclusion; to ascertain the extent to which this inclusive approach, on paper, affords in-class and school-based support for gifted and talented/highly able learners. The results indicate that the legislative and policy frameworks coalesce with the Global Principles. While legislation does not change practice, it does influence and shape practice, and so can be used as a springboard for developing dynamic, culturally appropriate opportunities for Scotland’s gifted young people.

Biomarkers for Parkinson's disease (PD) diagnosis, prognostication and clinical trial cohort selection are an urgent need. While many promising markers have been discovered through the National Institute of Neurological Disorders and Stroke Parkinson's Disease Biomarker Program (PDBP) and other mechanisms, no single PD marker or set of markers are ready for clinical use. Here we discuss the current state of biomarker discovery for platforms relevant to PDBP. We discuss the role of the PDBP in PD biomarker identification and present guidelines to facilitate their development. These guidelines include: harmonizing procedures for biofluid acquisition and clinical assessments, replication of the most promising biomarkers, support and encouragement of publications that report negative findings, longitudinal follow-up of current cohorts including the PDBP, testing of wearable technologies to capture readouts between study visits and development of recently diagnosed ( ) cohorts to foster identification of the earliest markers of disease onset.

Early years and primary settings are increasingly required to identify and challenge their gifted pupils. This book, by a hugely popular author, explains how to do just that and provides lots of activities and guidance.

Galectins are pleiotropic carbohydrate-binding lectins involved in inflammation, growth/differentiation, and tissue remodeling. The functional role of galectins in amyotrophic lateral sclerosis (ALS) is unknown. Expression studies revealed increases in galectin-1 mRNA and protein in spinal cords from SOD1(G93A) mice, and in galectin-3 and -9 mRNAs and proteins in spinal cords of both SOD1(G93A) mice and sporadic ALS patients. As the increase in galectin-3 appeared in early presymptomatic stages and increased progressively through to end stage of disease in the mouse, it was selected for additional study, where it was found to be mainly expressed by microglia. Galectin-3 antagonists are not selective and do not readily cross the blood-brain barrier; therefore, we generated SOD1(G93A)/Gal-3(-/-) transgenic mice to evaluate galectin-3 deletion in a widely used mouse model of ALS. Disease progression, neurological symptoms, survival, and inflammation were assessed to determine the effect of galectin-3 deletion on the SOD1(G93A) disease phenotype. Galectin-3 deletion did not change disease onset, but resulted in more rapid progression through functionally defined disease stages, more severely impaired neurological symptoms at all stages of disease, and expiration, on average, 25 days earlier than SOD1(G93A)/Gal-3(+/+) cohorts. In addition, microglial staining, as well as TNF-α, and oxidative injury were increased in SOD1(G93A)/Gal-3(-/-) mice compared with SOD1(G93A)/Gal-3(+/+) cohorts. These data support an important functional role for microglial galectin-3 in neuroinflammation during chronic neurodegenerative disease. We suggest that elevations in galectin-3 by microglia as disease progresses may represent a protective, anti-inflammatory innate immune response to chronic motor neuron degeneration.Galectins are pleiotropic carbohydrate-binding lectins involved in inflammation, growth/differentiation, and tissue remodeling. The functional role of galectins in amyotrophic lateral sclerosis (ALS) is unknown. Expression studies revealed increases in galectin-1 mRNA and protein in spinal cords from SOD1(G93A) mice, and in galectin-3 and -9 mRNAs and proteins in spinal cords of both SOD1(G93A) mice and sporadic ALS patients. As the increase in galectin-3 appeared in early presymptomatic stages and increased progressively through to end stage of disease in the mouse, it was selected for additional study, where it was found to be mainly expressed by microglia. Galectin-3 antagonists are not selective and do not readily cross the blood-brain barrier; therefore, we generated SOD1(G93A)/Gal-3(-/-) transgenic mice to evaluate galectin-3 deletion in a widely used mouse model of ALS. Disease progression, neurological symptoms, survival, and inflammation were assessed to determine the effect of galectin-3 deletion on the SOD1(G93A) disease phenotype. Galectin-3 deletion did not change disease onset, but resulted in more rapid progression through functionally defined disease stages, more severely impaired neurological symptoms at all stages of disease, and expiration, on average, 25 days earlier than SOD1(G93A)/Gal-3(+/+) cohorts. In addition, microglial staining, as well as TNF-α, and oxidative injury were increased in SOD1(G93A)/Gal-3(-/-) mice compared with SOD1(G93A)/Gal-3(+/+) cohorts. These data support an important functional role for microglial galectin-3 in neuroinflammation during chronic neurodegenerative disease. We suggest that elevations in galectin-3 by microglia as disease progresses may represent a protective, anti-inflammatory innate immune response to chronic motor neuron degeneration.

The Extracellular RNA (exRNA) Communication Consortium, funded as an initiative of the NIH Common Fund, represents a consortium of investigators assembled to address the critical issues in the exRNA research arena. The overarching goal is to generate a multi-component community resource for sharing fundamental scientific discoveries, protocols, and innovative tools and technologies. The key initiatives include (a) generating a reference catalogue of exRNAs present in body fluids of normal healthy individuals that would facilitate disease diagnosis and therapies, (b) defining the fundamental principles of exRNA biogenesis, distribution, uptake, and function, as well as development of molecular tools, technologies, and imaging modalities to enable these studies, (c) identifying exRNA biomarkers of disease, (d) demonstrating clinical utility of exRNAs as therapeutic agents and developing scalable technologies required for these studies, and (e) developing a community resource, the exRNA Atlas, to provide the scientific community access to exRNA data, standardized exRNA protocols, and other useful tools and technologies generated by funded investigators.

The present paper provides an overview of the current national legislation, policies, curriculum and practice relating to gifted education within Scotland. It begins by providing an overview of the national context and historical background that, to this day, underpin the egalitarian ethos that permeates Scottish education. We discuss how historical, philosophical and political narratives that are firmly rooted in the belief that education is a right for all foreshadow Scotland's approach to \"gifted education\". The legislative shift within Scotland from a \"needs-based\" model to a \"rights-based\" model, coupled with our inclusive approach to education for all, has important implications and provides potential opportunities for gifted young people. The strengths and limitations of this approach are debated within the paper. Rhetoric and reality can, however, be unfamiliar strangers; the paper therefore also aims to demonstrate how legislative intention and pedagogical ideals have been put into practice within Scottish schools in order to meet the needs of gifted young Scots. We conclude by discussing the challenges that remain and the implications for the future, both within and beyond Scotland. (DIPF/Orig.).

Andrew Singleton and colleagues report a large-scale meta-analysis of genome-wide association data in Parkinson's disease using over 13,000 cases and 95,000 controls plus additional samples for replication. They identify 6 new risk loci and replicate 28 independent risk variants for Parkinson's disease across 24 loci. We conducted a meta-analysis of Parkinson's disease genome-wide association studies using a common set of 7,893,274 variants across 13,708 cases and 95,282 controls. Twenty-six loci were identified as having genome-wide significant association; these and 6 additional previously reported loci were then tested in an independent set of 5,353 cases and 5,551 controls. Of the 32 tested SNPs, 24 replicated, including 6 newly identified loci. Conditional analyses within loci showed that four loci, including GBA , GAK - DGKQ , SNCA and the HLA region, contain a secondary independent risk variant. In total, we identified and replicated 28 independent risk variants for Parkinson's disease across 24 loci. Although the effect of each individual locus was small, risk profile analysis showed substantial cumulative risk in a comparison of the highest and lowest quintiles of genetic risk (odds ratio (OR) = 3.31, 95% confidence interval (CI) = 2.55–4.30; P = 2 × 10 −16 ). We also show six risk loci associated with proximal gene expression or DNA methylation.

Purpose Impact investment is an emergent field worldwide and it can play an especially important role in Africa. The aim of this study was to examine how impact investors in South Africa manage the tensions between financial returns and social impact. Design/methodology/approach The research was based on 15 semi-structured interviews with key stakeholders in the impact investment community in South Africa to understand the related challenges, trade-offs and tensions. Findings There are two opposing views expressed as to whether the tensions between financial return and social impact result in trade-offs. It is proposed that impact investors embrace this duality and seek to approach it through a contingency and a paradox view. The tensions can be approached by focussing on values alignment, contracting processes, engaged leadership and sector identification. The authors integrate the findings into a proposed framework for effective tension management in an impact investment portfolio. Research limitations/implications This study was limited to selected South African interviewees. It would be valuable to extend the study to other African countries. Practical implications The issue of values alignment between investors, fund managers and investee firms is an important finding for practice. As is the four-part iterative framework for sensing the operating environment, defining impact, organising internally and defining the investment approach. Originality/value This study contributes empirical evidence to scholarship around organisational tensions, especially work in hybrid organisations. It affirms the value of a nuanced application of paradox theory. It examines these tensions through the lived experience of impact investing professionals in an emerging market context.

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