Family language policy and planning in China::the changing langscape

In this editorial introduction, we present what motivated us to organise this collection of studies on family language policy and planning (FLPP) in the Chinese contexts. In order to better understand why ethnic minority languages and fangyans (also known as dialects or regionalects) are challenged by the official Chinese language, Putonghua, the introduction situates this group of studies in the disciplinary context, and proposes the family as a critical site where macro and meso language policies penetrate the private domain and influence the process of family language decisions. By looking at the interactions between families, schools, communities and workplaces, we can also trace the sociolinguistic and political environments in which language shift takes place. In the discussion of these contextual factors in China, we argue for the need to explore family and language changes in Chinese contexts. The introduction concludes with an overview of the studies included in this special issue, highlighting the key claims put forward by the contributors

A Framework for Designing Learning Analytics Information Systems

Learning analytics offers new opportunities in higher education, yet the design and development of educational data analytics are facing several challenges. Little guidance is available for researchers and developers when it comes to designing, developing, and implementing learning analytics information systems in higher education. Hence, this study proposes a comprehensive conceptual framework for designing learning analytics information systems incorporating both computational and educational aspects. The framework provides systematic support for learning analytics researchers and designers. It is constructed based on the process and critical dimensions of learning analytics and instructional systems design. By applying the framework to analyze a previously published study, we provide a better understanding of its key qualities. Furthermore, the application of the framework to design a new learning analytics information system provides forward engineering support

A Novel Method for Calculating the Radiated Disturbance from Pantograph Arcing in High-speed Railway

Pantograph arcing is a key electromagnetic disturbance source to affect train control system in high-speed railway. Since the characteristics of pantograph arcing is related to train speed, it is necessary to investigate effective numerical modeling and measurement method. However, due to the uncontrollable train speed during on-site measurement, it is difficult to study the radiated disturbance from arcing in the corresponding speed and repeat the same measurement. Therefore, a method combined numerical modeling and reverberation chamber measurements for calculating the radiated disturbance from pantograph arcing in a high-speed railway is proposed. Numerical models of train and sensitive equipment are built to calculate the coupling coefficient in CONCEPT II. And a new measurement procedure in reverberation chamber using pulse signal as the reference source is proposed based on a speed-controllable laboratory replica to measure the total radiated power of pantograph arcing. Then the radiated disturbance from pantograph arcing to the sensitive equipment is achieved with the coupling coefficient and the total radiated power of arcing. The method is verified laboratory experiments. This method can solve the uncontrollable train speed problem during on-site measurement and improve the repeatability of measurement

Chronic social defeat stress shifts peripheral circadian clocks in male mice in a tissue-specific and time-of-day dependent fashion

Uncontrollable stress is linked to the development of many diseases, some of which are associated with disrupted daily rhythms in physiology and behavior. While available data indicate that the master circadian pacemaker in the suprachiasmatic nucleus (SCN) is unaffected by stress, accumulating evidence suggest that circadian oscillators in peripheral tissues and organs can be shifted by a variety of stressors and stress hormones. In the present study, we examined effects of acute and chronic social defeat stress in mice and addressed the question of whether effects of uncontrollable stress on peripheral clocks are tissue specific and depend on time of day of stress exposure. We used mice that carry a luciferase reporter gene fused to the circadian clock gene Period2 (PER2::LUC) to examine daily rhythms of PER2 expression in various peripheral tissues. Mice were exposed to social defeat stress in the early (ZT13-14) or late (ZT21-22) dark phase, either once (acute stress) or repeatedly on 10 consecutive days (chronic stress). One hour after the last stressor, tissue samples from liver, lung, kidney, and white adipose tissue (WAT) were collected. Social defeat stress caused a phase delay of several hours in the rhythm of PER2 expression in lung and kidney, but this delay was stronger after chronic than after acute stress. Moreover, shifts only occurred after stress in the late dark phase, not in the early dark phase. PER2 rhythms in liver and WAT were not significantly shifted by social defeat, suggesting a different response of various peripheral clocks to stress. This study indicates that uncontrollable social defeat stress is capable of shifting peripheral clocks in a time of day dependent and tissue specific manner. These shifts in peripheral clocks were smaller or absent after a single stress exposure and may therefore be the consequence of a cumulative chronic stress effect

Current-Smoking alters Gene Expression and DNA Methylation in the Nasal Epithelium of Asthmatics

Current-smoking contributes to worsened asthma prognosis, more severe symptoms and limits the beneficial effects of corticosteroids. As the nasal epithelium can reflect smoking-induced changes in the lower airways, it is a relevant source to investigate changes in gene expression and DNA methylation. This study explores gene expression and DNA methylation changes in current and ex-smokers with asthma. Matched gene expression and epigenome-wide DNA methylation samples collected from nasal brushings of 55 patients enrolled in a clinical trial investigation of current and ex-smoker asthma patients were analysed. Differential gene expression and DNA methylation analyses were conducted comparing current- vs ex-smokers. Expression quantitative trait methylation (eQTM) analysis was completed to explore smoking relevant genes by CpG sites that differ between current and ex-smokers. To investigate the relevance of the smoking-associated DNA methylation changes for the lower airways, significant CpG sites were explored in bronchial biopsies from patients who had stopped smoking. 809 genes and 18,814 CpG sites were differentially associated with current-smoking in the nose. The cis-eQTM analysis uncovered 171 CpG sites whose methylation status associated with smoking-related gene expression, including AHRR, ALDH3A1, CYP1A1 and CYP1B1. Methylation status of CpG sites altered by current-smoking reversed with one-year smoking cessation. We confirm current-smoking alters epigenetic patterns and affects gene expression in the nasal epithelium of asthma patients, which is partially reversible in bronhcial biopsies after smoking cessation. We demonstrate the ability to discern molecular changes in the nasal epithelium, presenting this as a tool in future investigations into disease-relevant effects of tobacco smoke

Drought cuts back regeneration in logged tropical forests

Logged tropical forests represent a major opportunity for preserving biodiversity and sequestering carbon, playing a large role in meeting global forest restoration targets. Left alone, these ecosystems have been expected to undergo natural regeneration and succession towards old growth forests, but extreme drought events may challenge this process. While old growth forests possess a certain level of resilience, we lack understanding as to how logging may affect forest responses to drought. This study examines the drought–logging interaction in seedling dynamics within a landscape of logged and unlogged forests in Sabah Malaysia, based on 73 plots monitored before and after the 2015-16 El Niño drought. Drought increased seedling mortality in all forests, but the magnitude of this impact was modulated by logging intensity, with forests with lower canopy leaf area index (LAI) and above ground biomass (AGB) experiencing greater drought induced mortality. Moreover, community traits in more heavily logged forests shifted towards being more ruderal after drought, suggesting that the trajectory of forest succession had been reversed. These results indicate that with reoccurring strong droughts under a changing climate, logged forests that have had over half of their biomass removed may suffer permanently arrested succession. Targeted management interventions may therefore be necessary to lift the vulnerable forests above the biomass threshold

A genetic variation map for chicken with 2.8 million single-nucleotide polymorphisms

We describe a genetic variation map for the chicken genome containing 2.8 million single-nucleotide polymorphisms ( SNPs). This map is based on a comparison of the sequences of three domestic chicken breeds ( a broiler, a layer and a Chinese silkie) with that of their wild ancestor, red jungle fowl. Subsequent experiments indicate that at least 90% of the variant sites are true SNPs, and at least 70% are common SNPs that segregate in many domestic breeds. Mean nucleotide diversity is about five SNPs per kilobase for almost every possible comparison between red jungle fowl and domestic lines, between two different domestic lines, and within domestic lines - in contrast to the notion that domestic animals are highly inbred relative to their wild ancestors. In fact, most of the SNPs originated before domestication, and there is little evidence of selective sweeps for adaptive alleles on length scales greater than 100 kilobases

HERON: Demonstrating a Novel Biological Platform for Small Satellite Missions

Long-duration deep space missions pose a significant health risk for both humans and their resident microorganisms. The GeneSat, PharmaSat and O/OREOS missions have previously explored biological questions regarding the effects of spaceflight on S. cerevisiase, B. subtilis, and E. coli. However, there currently exists both a knowledge and an accessibility gap in small satellite biological experiments. These payloads require precise instrumentation and complex platforms that are usually reserved for large research organizations. This makes it difficult for smaller organizations to perform biological research in low Earth orbit (LEO). To address these challenges, the University of Toronto Aerospace Team (UTAT) Space Systems Division is currently developing the HERON CubeSat. HERON houses a payload platform which measures the effects of the LEO environment on the gene expression and drug resistance of Candida albicans, a yeast commonly found in the human gut microbiome. Previous research has suggested that C. albicans might display increased pathogenicity and drug resistance in response to microgravity, which has important implications for long-duration human spaceflight. The yeast cells are housed in custom acrylic microfluidics chips containing 32 wells with channels for media and drug delivery. A measurement printed circuit board (PCB) contains custom optics capable of measuring minute changes in cell fluorescence. The entire payload stack is then housed in a temperature- and humidity-controlled 2U pressure vessel. Space Systems as a whole is an undergraduate student-led and student-funded design team, dedicated to the development of small satellite missions with a focus on education and undergraduate learning. HERON is scheduled to launch Q1 2022 into a Sun-synchronous orbit via a SpaceX Falcon 9 rocket at an altitude of approximately 550 km. Our platform is open-source and can serve as a low-cost template for future biological CubeSat missions. This paper serves as a technical and scientific description of the platform, along with the lessons learned during the payload design, assembly, and validation processes

Epithelial NEMO links innate immunity to chronic intestinal inflammation

Deregulation of intestinal immune responses seems to have a principal function in the pathogenesis of inflammatory bowel disease(1-4). The gut epithelium is critically involved in the maintenance of intestinal immune homeostasis-acting as a physical barrier separating luminal bacteria and immune cells, and also expressing antimicrobial peptides(3,5,6). However, the molecular mechanisms that control this function of gut epithelial cells are poorly understood. Here we show that the transcription factor NF kappa B, a master regulator of pro-inflammatory responses(7,8), functions in gut epithelial cells to control epithelial integrity and the interaction between the mucosal immune system and gut microflora. Intestinal epithelial-cell-specific inhibition of NF-kappa B through conditional ablation of NEMO ( also called I kappa B kinase-gamma ( IKK gamma)) or both IKK1 ( IKK alpha) and IKK2 ( IKK beta)-IKK subunits essential for NF-kappa B activation(7-9)-spontaneously caused severe chronic intestinal inflammation in mice. NF-kappa B deficiency led to apoptosis of colonic epithelial cells, impaired expression of antimicrobial peptides and translocation of bacteria into the mucosa. Concurrently, this epithelial defect triggered a chronic inflammatory response in the colon, initially dominated by innate immune cells but later also involving T lymphocytes. Deficiency of the gene encoding the adaptor protein MyD88 prevented the development of intestinal inflammation, demonstrating that Toll-like receptor activation by intestinal bacteria is essential for disease pathogenesis in this mouse model. Furthermore, NEMO deficiency sensitized epithelial cells to tumour-necrosis factor ( TNF)-induced apoptosis, whereas TNF receptor-1 inactivation inhibited intestinal inflammation, demonstrating that TNF receptor-1 signalling is crucial for disease induction. These findings demonstrate that a primary NF-kappa B signalling defect in intestinal epithelial cells disrupts immune homeostasis in the gastrointestinal tract, causing an inflammatory-bowel-disease-like phenotype. Our results identify NF-kappa B signalling in the gut epithelium as a critical regulator of epithelial integrity and intestinal immune homeostasis, and have important implications for understanding the mechanisms controlling the pathogenesis of human inflammatory bowel disease.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/62858/1/nature05698.pd