Miracle-dz/UniFAR-FTUs huggingface dataset:
Reflecting on the creativity agenda in education

Among the initiatives, scholarly conversations, and recent events which demonstrate the ongoing salience of the creativity agenda in education has been a series of six seminars. The seminar series, an initiative of the British Educational Research Association Special Interest Group (BERA SIG), Creativity in Education was held between September 2003 and December 2005. In April 2005, I co-organized and chaired the seminar entitled ‘Creativity: using it wisely? ’ This involved keynote speakers: Howard Gardner, Harvard University, Guy Claxton, University of Bristol and Anna Craft, The Open University. This seminar, hosted by the Faculty of Education, University of Cambridge, attracted 180 delegates including researchers, practitioners and policy-makers with the purpose of sharing situated perspectives on (and some rethinking of) creativity in education. This event was coupled with a twoday residential International Symposium on Creative Learning. The contributors to this special issue were linked to both the seminar and symposium from which papers were submitted by the keynote speakers, presenters and discussants and then refereed according to standard Cambridge Journal of Education procedures. The timeliness of this special issue is embedded in an unprecedented resurgence of activity in the field of creativity in education as an area of scholarship, as a key element of the shifting education policy context, and official agenda in relation to efforts to improve our schools. The creativity agenda is recognized in many countries—not as a transient fad, but as having an explicit role in the economy. It therefore constitutes a fundamentally political imperative. Yet the informing contexts and desired outcomes that characterize creativity as a valued human capacity remain elusive. Consequently, its individual, institutional and cultural value and purpose remain vigorously debated issues (Csikszentmihalyi, 1996; JohnSteiner, 2000; Runco, 2002; Sternberg, 2003; Craft, 2005). There is great public deliberation and publicity around the creativity agenda, especially but not only in the UK. In England a great deal of energy (and funding) is devoted to conceptualizing and developing both learning and pedagogy. The agenda is situated and played out in a variety of development work in schools and elsewhere, supported through a range of organizations including Creative Partnerships (Creative Partnerships & DEMOS, 2003; Creative Partnerships, 2004a, b), National College Cambridge Journal of Education Vol. 36, No. 3, September 2006, pp. 313–318
Implications of Cellular Aging in Cardiac Reprogramming

Aging is characterized by a chronic functional decline of organ systems which leads to tissue dysfunction over time, representing a risk factor for diseases development, including cardiovascular. The aging process occurring in the cardiovascular system involves heart and vessels at molecular and cellular level, with subsequent structural modifications and functional impairment. Several modifications involved in the aging process can be ascribed to cellular senescence, a biological response that limits the proliferation of damaged cells. In physiological conditions, the mechanism of cellular senescence is involved in regulation of tissue homeostasis, remodeling, and repair. However, in some conditions senescence-driven tissue repair may fail, leading to the tissue accumulation of senescent cells which in turn may contribute to tumor promotion, aging, and age-related diseases. Cellular reprogramming processes can reverse several age-associated cell features, such as telomere length, DNA methylation, histone modifications and cell-cycle arrest. As such, induced Pluripotent Stem Cells (iPSCs) can provide models of progeroid and physiologically aged cells to gain insight into the pathogenesis of such conditions, to drive the development of new therapies for premature aging and to further explore the possibility of rejuvenating aged cells. An emerging picture is that the tissue remodeling role of cellular senescence could also be crucial for the outcomes of in vivo reprogramming processes. Experimental evidence has demonstrated that, on one hand, senescence represents a cell-autonomous barrier for a cell candidate to reprogramming, but, on the other hand, it may positively sustain the reprogramming capability of surrounding cells to generate fully proficient tissues. This review fits into this conceptual framework by highlighting the most prominent concepts that characterize aging and reprogramming and discusses how the aging tissue might provide a favorable microenvironment for in vivo cardiac reprogramming.
An energy efficient approach to virtual machines management in cloud computing

Cloud computing platforms are well established as the reference infrastructure for flexibility allowing business to scale according to user demands. However, several challenges remain to be addressed. Scaling up the infrastructure to match up the resource demand of the users is relatively straight forward. However in order to save up on power consumption, cloud providers have to dynamically consolidate the virtual machines (VM), so that only a reduced subset of hosts remains powered on. To solve this issue, the cloud scheduler, which handles the VM allocations, has to balance between providing enough resource to each user, and reducing the overall power consumption of the cloud. In this paper we investigate the VM allocation and reallocation inside a cloud in order to save energy while maintaining the resources required by users. Such actions have to be made in order to minimize the number of hosts powered on, while limiting concurrent migrations of virtual machines, and in a reasonable computational time. We propose to effectively consolidate virtual machines with an approach handling the reallocation, migration and host management problems. Our approach has been implemented in OpenNebula, and experimentally compared with its default approach.
Surfactant proteins and inflammation: the yin and the yang.

Alveolar surfactant is a complex mixture of lipids and proteins that executes two disparate functions. First, surfactant reduces surface tension at the air–liquid interface of the lung thereby preventing lung collapse. Second, surfactant functions in pulmonary host defense. The host defense functions are mediated primarily by the hydrophilic protein constituents of surfactant, surfactant protein (SP)-A and SP-D (1–3). SP-A and SP-D are members of a family of proteins known as collectins, or collagenlike lectins (3), all of which have a four-domain primary structure consisting of a disulfide-forming NH2 terminus, a collagen-like region, a coiled neck region, and a COOH-terminal carbohydrate recognition domain (4). SP-A and SP-D bind via their carbohydrate recognition domains to sugar and glycolipid residues on microbial cell walls. SP-A and SP-D form trimers and oligomers, which greatly increase their valence and efficiency at binding pathogens (3). Both SP-A and SP-D have been shown to mediate phagocytosis and killing of pathogens both in vivo and in vitro (reviewed in Refs. 3 and 5). Transgenic mice, deficient in SP-A and SP-D, have enhanced susceptibility to bacterial and viral infections and develop more severe pulmonary lesions than do wild-type mice after inoculation of their lungs with various pathogens (reviewed in Refs. 3 and 5). A point of some controversy in the field has been whether SP-A and SP-D enhance or inhibit production of inflammatory mediators. The focus of this Perspective is to briefly summarize this controversy and to highlight new findings in the area, including those of Wu and coworkers published in this issue of AJRCMB (6), that provide some resolution to this controversy. Several lines of evidence show that SP-A either enhances or decreases the production of reactive nitrogen and inflammatory cytokines by immune cells. For example, SP-A enhanced the production of NO and nitric oxide synthase (NOS)2 (inducible NOS) expression in rat alveolar macrophages (AMs), previously activated with interferon , but inhibited NO production and NOS2 expression by lipopolysaccharide (LPS)-activated macrophages (7). SP-A may exert differential effects depending on the type of stimulus or pathogen presented to the cell. For example, SP-A reduced the production of NO by AMs in the presence of Mycobacterium tuberculosis, and this was correlated with reduced killing of organisms (8). In contrast, SP-A enhanced the
24 Complications of Liver Biopsy

The liver is the second largest organ in the body after the skin and has important storage, detoxification and synthetic functions. Liver diseases encompass a multitude of pathologies and the management of these diseases involves diagnostic and therapeutic investigations and interventions; some of which are invasive. Histological assessment of the liver and lesions within via liver biopsies are an important tool in the armamentarium of invasive investigations for liver diseases of both a surgical and non-surgical nature. Liver biopsy has been used for over 100 years in the assessment of liver diseases (Valori and Elias 1989). Paul Ehrlich performed one of the first percutaneous liver biopsies in the late 19th century in Germany to assess glycogen levels in the liver of a diabetic patient (Grant and Neuberger 1999). However, the procedure did not really gain popularity until Menghini refined the technique in the mid 20th century(Menghini 1958). In the last fifty years the techniques for liver biopsy has been continuously refined and although today there are several biochemical and imaging techniques to assess liver disease biopsy remains important in assessment. Today, widespread application allows for blind, open and image guided liver biopsies, although ultrasound guided biopsies are considered superior (Younossi, Teran, Ganiats and Carey 1998). Image guided percutaneous liver biopsies remains the mainstay of this procedure while open biopsies may be undertaken as an adjunct to laparoscopic or other open surgical procedures. There are presently various techniques and equipment for percutaneous liver biopsies and this procedure is performed by both gastroenterologists/hepatologists and radiologists. The choice of technique and equipment is however operator dependent.
Editorial: genotype 3 HCV—who still needs ribavirin in a pan‐genotypic era? Authors’ reply

We read with interest the editorial provided by Dr. Sadler on our manuscript reporting real-world experience with sofosbuvir and velpatasvir (SOF/VEL) and the impact of baseline resistance associated substitutions in the nonstructural protein 5A (NS5A RASs) on treatment outcome in patients with chronic hepatitis C (HCV) genotype 3 infection (GT3). Dr. Sadler assessed the prevalence of high level NS5A RASs in our study as too low to draw meaningful conclusions regarding their impact on treatment outcome. However, we would like to emphasise that the prevalence of NS5A RASs in our study was effectively comparable to that reported in clinical trials of SOF/ VEL for HCV GT3. In a pooled analysis of the ASTRAL studies, 12% of GT3 patients (57 of 476 patients) had any baseline NS5A RASs and 4.6% had a Y93H RAS (22 of 476 patients), compared to 11.2% and 4.6%, respectively, in our study. This surely might be explained by the fact that most patients had not received an NS5A inhibitor before. Moreover, our data are complemented by a recent real-world study from several European countries, including Germany, Switzerland and Austria, that showed a 9% NS5A RASs prevalence in 375 DAA-na€ıve GT3 patients. Therefore, we believe that our study population adequately mirrors the prevalence of NS5A RASs in the Western GT3 population. More importantly, our results suggest that their impact on treatment outcome may be less striking than previously reported, particularly in patients without cirrhosis. Regarding the use of ribavirin in patients with compensated cirrhosis, we agree with Dr. Sadler on the limited conclusions that can be drawn from our study. A definite answer to this question would require a controlled, randomised trial, which is unlikely to be conducted given the overall high SVR rates with modern DAA regimens. We also agree that the use of ribavirin is required in patients with decompensated cirrhosis; a recommendation based on the ASTRAL-4 clinical trial and now further underscored by our results with notably even higher SVR rates. Concerning the importance of ribavirin in patients without cirrhosis but baseline NS5A RAS probably studies in larger patient cohorts may be required to draw definite conclusions. Currently, our findings do not support the general use of ribavirin in GT3 patients without cirrhosis, irrespective of the presence of baseline NS5A RAS. Further our results suggest that ribavirin may not be necessary in most DAA-na€ıve patients with compensated cirrhosis considering the high SVR rates in this subgroup treated without ribavirin. However, the role of SOF/VEL plus ribavirin after DAA failure as a possible treatment alternative to, for example, SOF/VEL plus voxilaprevir certainly requires further investigation in the real-world setting. ACKNOWLEDGEMENTS
Optimal Symmetric No-Trade Ranges in Asset Rebalancing Strategy with Transaction Costs

There are many studies of optimal asset allocation with transaction costs in academic literatures. However, those are numerically solved for two-asset and three-asset cases. In contrast, the investment in five-asset classes (domestic bond and stock, international bond and stock, and cash) is at least required for practical pension fund management. Therefore, there are some real limitations to the continuous-time approach used in the previous literatures, which are the methods of solving the Hamilton-Bellman-Jacobi (HJB) equation for the stochastic control problem. In general, most investors use the rebalance rule with the no-trade ranges in practice which are constant and symmetric to the policy asset mix because it is easy to use the rule. In this paper, we propose the optimization model for the multiple asset allocation problem with transaction costs to determine the symmetric no-trade ranges of the policy asset mix using the derivative-free optimization (DFO) approach proposed by Hibiki et al. (2014). Specifically, we solve the five-asset problem with boundary constraints for cash for the Government Pension Investment Fund (GPIF) in Japan in a discrete-time and finite-period setting. We clarify the fact that we need to adjust the amounts of risky assets even within the no-trade range if the boundary constraints for cash are required, and we describe the simulation procedure in the discrete-time model. We examine the difference for various time intervals and horizons and conduct the sensitivity analysis for the various proportional transaction cost rates, the tracking error aversions, and the bounds for cash constraints. In addition, we compare the optimal time-dependent no-trade ranges with the constant no-trade ranges. The numerical results show the possibilities of applying the DFO model to the practical problem determining the symmetric no-trade ranges.
Final WP 4 report on testbeds and field-trials

WP4 coordinates experimental activities, with imple mentation and testing of the technologies and procedures studied in the project. This report c vers the progress made during the last (third) year of the project. Keyword list: yearly, final, activities, experimental, testbeds, field-trials FP7-ICT-257740/ D4.5 Page 2 of 41 Disclaimer The information, documentation and figures available in this deliverable are written by the TREND Consortium partners under EC co-financing (project FP7-ICT-257740) and does not necessarily reflect the view of the European Commission. The information in this document is provided "as is", and no guarantee or warranty is given that the information is fit for any particular purpose. The user uses the information at its sole risk and liability. FP7-ICT-257740/ D4.5 Page 3 of 41 Table of
Pediatric diffuse midline glioma H3K27- altered: A complex clinical and biological landscape behind a neatly defined tumor type

The 2021 World Health Organization Classification of Tumors of the Central Nervous System, Fifth Edition (WHO-CNS5), has strengthened the concept of tumor grade as a combination of histologic features and molecular alterations. The WHO-CNS5 tumor type “Diffuse midline glioma, H3K27-altered,” classified within the family of “Pediatric-type diffuse high-grade gliomas,” incarnates an ideally perfect integrated diagnosis in which location, histology, and genetics clearly define a specific tumor entity. It tries to evenly characterize a group of neoplasms that occur primarily in children and midline structures and that have a dismal prognosis. Such a well-defined pathological categorization has strongly influenced the pediatric oncology community, leading to the uniform treatment of most cases of H3K27-altered diffuse midline gliomas (DMG), based on the simplification that the mutation overrides the histological, radiological, and clinical characteristics of such tumors. Indeed, multiple studies have described pediatric H3K27-altered DMG as incurable tumors. However, in biology and clinical practice, exceptions are frequent and complexity is the rule. First of all, H3K27 mutations have also been found in non-diffuse gliomas. On the other hand, a minority of DMGs are H3K27 wild-type but have a similarly poor prognosis. Furthermore, adult-type tumors may rarely occur in children, and differences in prognosis have emerged between adult and pediatric H3K27-altered DMGs. As well, tumor location can determine differences in the outcome: patients with thalamic and spinal DMG have significantly better survival. Finally, other concomitant molecular alterations in H3K27 gliomas have been shown to influence prognosis. So, when such additional mutations are found, which one should we focus on in order to make the correct clinical decision? Our review of the current literature on pediatric diffuse midline H3K27-altered DMG tries to address such questions. Indeed, H3K27 status has become a fundamental supplement to the histological grading of pediatric gliomas; however, it might not be sufficient alone to exhaustively define the complex biological behavior of DMG in children and might not represent an indication for a unique treatment strategy across all patients, irrespective of age, additional molecular alterations, and tumor location.
Is bacterial translocation involved in the pathogenesis of idiopathic Non Cirrhotic Intrahepatic Portal Hypertension

INTRODUCTION : Non cirrhotic intrahepatic portal hypertension (NCIPH) is traditionally named as non cirrhotic portal fibrosis (NCPF) in India. It is more prevalent in developing countries and it is a commonly encountered clinical entity. As per data from our centre, cryptogenic cirrhosis is the commonest cause for portal hypertension, 39 to 48% of patients labeled as cryptogenic cirrhosis turn out to be NCIPH after liver biopsy. NCIPH usually appears to have a benign course, however patients may worsen to a stage requiring liver transplantation. The exact etiopathogenesis of this common condition is still unknown. There are various hypotheses like infective, immunogenic, prothrombotic and trace elements exposure. There are data to support the association between gut disorders, prothrombotic conditions and NCIPH. Eapen et al found 16% of NCIPH patients to have celiac disease and 3% to have ulcerative colitis. Hillaire et al found association between prothrombotic conditions like myeloproliferative disorders and NCIPH. Considering the above associations, we postulate a hypothesis that a combined effect of gut disorders and prothrombotic conditions lead to portal microangiopathy. Gut disorders like celiac disease are commonly associated with altered intestinal permeability called as leaky gut. This leakiness can lead to migration of bacteria and bacterial products from the gut which is termed as bacterial translocation. In the presence of a preexisting prothrombotic state in portal circulation, these gut factors could trigger a thrombotic event. It is well known that in liver cirrhosis, altered intestinal permeability and bacterial translocation happen, particularly in patients with ascites and advanced cirrhosis. AIM : 1. To study the association between gut disorders, bacterial translocation and NCIPH. 2. To assess the status of ADAMTS13 (a disintegrin and metalloprotease with a thrombospondin type 1 motif, member 13) in NCIPH patients and compare with that of controls. CONCLUSIONS : Most of the NCIPH patients had shrunken liver by imaging and almost half of them had a high HVPG suggesting that liver biopsy is essential to differentiate NCIPH from cryptogenic cirrhosis. Prevalence of celiac disease among NCIPH patients was noted to be 9.4% which is much higher than that reported among general population (upto 1%) Intestinal permeability was preserved in majority of patients both among cases and controls There was no rise in plasma TNF alpha levels both in cases and controls ADAMTS13 activity was found to be significantly low in NCIPH patients than in Controls ADAMTS13 antigen level was found to be significantly low in NCIPH patients than in controls Among patients with compensated liver disease (CTP A status) there was a significantly low ADAMTS13 activity and antigen level among NCIPH patients in comparison with controls. There was no correlation between ADAMTS13 activity and MELD score or HVPG.
Unsupervised Domain Adaptation with Global and Local Graph Neural Networks in Limited Labeled Data Scenario: Application to Disaster Management

Identification and categorization of social media posts generated during disasters are crucial to reduce the sufferings of the affected people. However, lack of labeled data is a significant bottleneck in learning an effective categorization system for a disaster. This motivates us to study the problem as unsupervised domain adaptation (UDA) between a previous disaster with labeled data (source) and a current disaster (target). However, if the amount of labeled data available is limited, it restricts the learning capabilities of the model. To handle this challenge, we utilize limited labeled data along with abundantly available unlabeled data, generated during a source disaster to propose a novel two-part graph neural network. The first-part extracts domain-agnostic global information by constructing a token level graph across domains and the second-part preserves local instance-level semantics. In our experiments, we show that the proposed method outperforms state-of-the-art techniques by $2.74\%$ weighted F$_1$ score on average on two standard public dataset in the area of disaster management. We also report experimental results for granular actionable multi-label classification datasets in disaster domain for the first time, on which we outperform BERT by $3.00\%$ on average w.r. t weighted F$_1$. Additionally, we show that our approach can retain performance when very limited labeled data is available.