Becoming an Expert, Ambassador or Doing Project Work: Three Paths to Excellence for Students at Artevelde University of Applied Sciences

Apart from the regular curricula in higher education, institutions increasingly offer additional initiatives or honours programmes for students to excel. Artevelde UAS wants to provide similar additional learning opportunities, in which the notion of excellence is based on reflection, self-direction and ‘giving back’ to stakeholders. This paper will provide an elaboration of these opportunities, based on three research questions: (1) What project or initiative can be considered as a valid and well-defined form of excelling, (2) How do we formally structure and organize this initiative or project, and (3) How can we evaluate and validate students’ experiences of excelling? Students of (International) Business Management at Artevelde UAS can excel in three different ways: by professionalizing and becoming an expert in a certain topic or area, by becoming an ambassador for one particular 21st century skill that has been put forward and highlighted by Artevelde UAS in its mission (global citizenship, entrepreneurship or sustainability), or by cooperating with professional business partners in order to develop and implement a real-life project.Lievens, B.; Cappelle, K.; Matthys, L. (2020). Becoming an Expert, Ambassador or Doing Project Work: Three Paths to Excellence for Students at Artevelde University of Applied Sciences. En 6th International Conference on Higher Education Advances (HEAd'20). Editorial Universitat Politècnica de València. (30-05-2020):985-992. https://doi.org/10.4995/HEAd20.2020.11184OCS98599230-05-202

An eco-friendly hybrid urban computing network combining community-based wireless LAN access and wireless sensor networking

Computer-enhanced smart environments, distributed environmental monitoring, wireless communication, energy conservation and sustainable technologies, ubiquitous access to Internet-located data and services, user mobility and innovation as a tool for service differentiation are all significant contemporary research subjects and societal developments. This position paper presents the design of a hybrid municipal network infrastructure that, to a lesser or greater degree, incorporates aspects from each of these topics by integrating a community-based Wi-Fi access network with Wireless Sensor Network (WSN) functionality. The former component provides free wireless Internet connectivity by harvesting the Internet subscriptions of city inhabitants. To minimize session interruptions for mobile clients, this subsystem incorporates technology that achieves (near-)seamless handover between Wi-Fi access points. The WSN component on the other hand renders it feasible to sense physical properties and to realize the Internet of Things (IoT) paradigm. This in turn scaffolds the development of value-added end-user applications that are consumable through the community-powered access network. The WSN subsystem invests substantially in ecological considerations by means of a green distributed reasoning framework and sensor middleware that collaboratively aim to minimize the network's global energy consumption. Via the discussion of two illustrative applications that are currently being developed as part of a concrete smart city deployment, we offer a taste of the myriad of innovative digital services in an extensive spectrum of application domains that is unlocked by the proposed platform

A murine intestinal intraepithelial NKp46-negative innate lymphoid cell population characterized by group 1 properties

The Ly49E receptor is preferentially expressed on murine innate-like lymphocytes, such as epidermal V gamma 3 T cells, intestinal intraepithelial CD8 alpha alpha(+) T lymphocytes, and CD49a(+) liver natural killer (NK) cells. As the latter have recently been shown to be distinct from conventional NK cells and have innate lymphoid cell type 1 (ILC1) properties, we investigated Ly49E expression on intestinal ILC populations. Here, we show that Ly49E expression is very low on known ILC populations, but it can be used to define a previously unrecognized intraepithelial innate lymphoid population. This Ly49E-positive population is negative for NKp46 and CD8 alpha alpha, expresses CD49a and CD103, and requires T-bet expression and IL-15 signaling for differentiation and/or survival. Transcriptome analysis reveals a group 1 ILC gene profile, different from NK cells, iCD8 alpha cells, and intraepithelial ILC1. Importantly, NKp46(-)CD8 alpha alpha(-)Ly49E(+) cells produce interferon (IFN)-gamma, suggesting that this previously unrecognized population may contribute to Th1-mediated immunity

Energy aware software evolution for wireless sensor networks

Wireless Sensor Networks (WSNs) are subject to high levels of dynamism arising from changing environmental conditions and application requirements. Reconfiguration allows software functionality to be optimized for current environmental conditions and supports software evolution to meet variable application requirements. Contemporary software modularization approaches for WSNs allow for software evolution at various granularities; from monolithic re-flashing of OS and application functionality, through replacement of complete applications, to the reconfiguration of individual software components. As the nodes that compose a WSN must typically operate for long periods on a single battery charge, estimating the energy cost of software evolution is critical. This paper contributes a generic model for calculating the energy cost of the reconfiguration in WSN. We have embedded this model in the LooCI middleware, resulting in the first energy aware reconfigurable component model for sensor networks. We evaluate our approach using two real-world WSN applications and find that (i.) our model accurately predicts the energy cost of reconfiguration and (ii.) component-based reconfiguration has a high initial cost, but provides energy savings during software evolution

AURORA : bariatric surgery registration in women of reproductive age : a multicenter prospective cohort study

C

The transcription factor ETS1 is an important regulator of human NK cell development and terminal differentiation

Natural killer (NK) cells are important in the immune defense against tumor cells and pathogens, and regulate other immune cells by cytokine secretion. Whereas murine NK cell biology has been extensively studied, knowledge about transcriptional circuitries controlling human NK cell development and maturation is limited. By generating ETS1-deficient human embryonic stem cells (hESC) and by expressing the dominant-negative ETS1 p27 isoform in cord blood (CB) hematopoietic progenitor cells (HPCs), we show that the transcription factor ETS1 is critically required for human NK cell differentiation. Genome-wide transcriptome analysis determined by RNA-sequencing combined with chromatin immunoprecipitation-sequencing (ChIP-seq) analysis reveals that human ETS1 directly induces expression of key transcription factors that control NK cell differentiation, i.e. E4BP4, TXNIP, TBET, GATA3, HOBIT and BLIMP1. In addition, ETS1 regulates expression of genes involved in apoptosis and NK cell activation. Our study provides important molecular insights into the role of ETS1 as an important regulator of human NK cell development and terminal differentiation

AURORA : bariatric surgery registration in women of reproductive age : a multicenter prospective cohort study

Background: The expansion of the obesity epidemic is accompanied with an increase in bariatric procedures, in particular in women of reproductive age. The weight loss induced by the surgery is believed to reverse the negative impact of overweight and obesity on female reproduction, however, research is limited to in particular retrospective cohort studies and a growing number of small case-series and case-(control) studies. Methods/design: AURORA is a multicenter prospective cohort study. The main objective is to collect long-term data on reproductive outcomes before and after bariatric surgery and in a subsequent pregnancy. Women aged 18-45 years are invited to participate at 4 possible inclusion moments: 1) before surgery, 2) after surgery, 3) before 15 weeks of pregnancy and 4) in the immediate postpartum period (day 3-4). Depending on the time of inclusion, data are collected before surgery (T1), 3 weeks and 3, 6, 12 or x months after surgery (T2-T5) and during the first, second and third trimester of pregnancy (T6-T8), at delivery (T9) and 6 weeks and 6 months after delivery (T10-T11). Online questionnaires are send on the different measuring moments. Data are collected on contraception, menstrual cycle, sexuality, intention of becoming pregnant, diet, physical activity, lifestyle, psycho-social characteristics and dietary supplement intake. Fasting blood samples determine levels of vitamin A, D, E, K, B-1, B-12 and folate, albumin, total protein, coagulation parameters, magnesium, calcium, zinc and glucose. Participants are weighted every measuring moment. Fetal ultrasounds and pregnancy course and complications are reported every trimester of pregnancy. Breastfeeding is recorded and breast milk composition in the postpartum period is studied. Discussion: AURORA is a multicenter prospective cohort study extensively monitoring women before undergoing bariatric surgery until a subsequent pregnancy and postpartum period

IRF2 is required for development and functional maturation of human NK cells

Natural killer (NK) cells are cytotoxic and cytokine-producing lymphocytes that play an important role in the first line of defense against malignant or virus-infected cells. A better understanding of the transcriptional regulation of human NK cell differentiation is crucial to improve the efficacy of NK cell-mediated immunotherapy for cancer treatment. Here, we studied the role of the transcription factor interferon regulatory factor (IRF) 2 in human NK cell differentiation by stable knockdown or overexpression in cord blood hematopoietic stem cells and investigated its effect on development and function of the NK cell progeny. IRF2 overexpression had limited effects in these processes, indicating that endogenous IRF2 expression levels are sufficient. However, IRF2 knockdown greatly reduced the cell numbers of all early differentiation stages, resulting in decimated NK cell numbers. This was not caused by increased apoptosis, but by decreased proliferation. Expression of IRF2 is also required for functional maturation of NK cells, as the remaining NK cells after silencing of IRF2 had a less mature phenotype and showed decreased cytotoxic potential, as well as a greatly reduced cytokine secretion. Thus, IRF2 plays an important role during development and functional maturation of human NK cells

Heterozygous Loss-of-Function SEC61A1 Mutations Cause Autosomal-Dominant Tubulo-Interstitial and Glomerulocystic Kidney Disease with Anemia

Autosomal-dominant tubulo-interstitial kidney disease (ADTKD) encompasses a group of disorders characterized by renal tubular and interstitial abnormalities, leading to slow progressive loss of kidney function requiring dialysis and kidney transplantation. Mutations in UMOD, MUC1, and REN are responsible for many, but not all, cases of ADTKD. We report on two families with ADTKD and congenital anemia accompanied by either intrauterine growth retardation or neutropenia. Ultrasound and kidney biopsy revealed small dysplastic kidneys with cysts and tubular atrophy with secondary glomerular sclerosis, respectively. Exclusion of known ADTKD genes coupled with linkage analysis, whole-exome sequencing, and targeted re-sequencing identified heterozygous missense variants in SEC61A1—c.553A>G (p.Thr185Ala) and c.200T>G (p.Val67Gly)—both affecting functionally important and conserved residues in SEC61. Both transiently expressed SEC6A1A variants are delocalized to the Golgi, a finding confirmed in a renal biopsy from an affected individual. Suppression or CRISPR-mediated deletions of sec61al2 in zebrafish embryos induced convolution defects of the pronephric tubules but not the pronephric ducts, consistent with the tubular atrophy observed in the affected individuals. Human mRNA encoding either of the two pathogenic alleles failed to rescue this phenotype as opposed to a complete rescue by human wild-type mRNA. Taken together, these findings provide a mechanism by which mutations in SEC61A1 lead to an autosomal-dominant syndromic form of progressive chronic kidney disease. We highlight protein translocation defects across the endoplasmic reticulum membrane, the principal role of the SEC61 complex, as a contributory pathogenic mechanism for ADTKD