Training manual for facilitators of teacher training seminars on education for responsible living

The Partnership for Education and Research about Responsible Living (PERL) comprises educators, researchers and practitioners from over 120 institutions in more than 50 countries. This partnership stems from an awareness of the urgent need for individuals and society to significantly rethink and reorient the choices they make and the manner in which they live their lives in order to reduce the negative impacts of climate change and financial instability, to ensure more just distribution of resources and to foster sustainable, dignified human development for all. Based on six years of work by the Consumer Citizenship Network (CCN), PERL partners develop projects, methods and materials to encourage people to contribute to constructive change through the way they choose to live. PERL is contributing to the Marrakech Process on Sustainable Consumption and Production, as well as to the UN Decade of Education for Sustainable Development (2005-2014), which boasts the active participation of UNEP, UNESCO, the Italian Task Force on Education for Sustainable Consumption and the Swedish Ministry of the Environment. PERL is based both in Europe as an Erasmus Academic Network and established in Asia Pacific, Africa and Latin America. The PERL network is a large multi-disciplinary organisation which has a core of working group members supported by a larger group which constitutes the Consultants network. PERL is coordinated from the Hedmark University College in Norway. The Norwegian Ministry of Children, Equality and Social Inclusion also supports PERL. One of the PERL working groups is focusing on ‘Active Learning Methodologies’ and its objectives are to develop resources that build on the criteria and student-centred constructive methods of the original “Images and Objects” Active Methodology Toolkit and the YouthXchange Training Kit.peer-reviewe

Neuregulin 1 and susceptibility to schizophrenia

To access full text version of this article. Please click on the hyperlink "View/Open" at the bottom of this pageThe cause of schizophrenia is unknown, but it has a significant genetic component. Pharmacologic studies, studies of gene expression in man, and studies of mouse mutants suggest involvement of glutamate and dopamine neurotransmitter systems. However, so far, strong association has not been found between schizophrenia and variants of the genes encoding components of these systems. Here, we report the results of a genomewide scan of schizophrenia families in Iceland; these results support previous work, done in five populations, showing that schizophrenia maps to chromosome 8p. Extensive fine-mapping of the 8p locus and haplotype-association analysis, supplemented by a transmission/disequilibrium test, identifies neuregulin 1 (NRG1) as a candidate gene for schizophrenia. NRG1 is expressed at central nervous system synapses and has a clear role in the expression and activation of neurotransmitter receptors, including glutamate receptors. Mutant mice heterozygous for either NRG1 or its receptor, ErbB4, show a behavioral phenotype that overlaps with mouse models for schizophrenia. Furthermore, NRG1 hypomorphs have fewer functional NMDA receptors than wild-type mice. We also demonstrate that the behavioral phenotypes of the NRG1 hypomorphs are partially reversible with clozapine, an atypical antipsychotic drug used to treat schizophrenia

The population genomic legacy of the second plague pandemic

Human populations have been shaped by catastrophes that may have left long-lasting signatures in their genomes. One notable example is the second plague pandemic that entered Europe in ca. 1,347 CE and repeatedly returned for over 300 years, with typical village and town mortality estimated at 10%–40%.1 It is assumed that this high mortality affected the gene pools of these populations. First, local population crashes reduced genetic diversity. Second, a change in frequency is expected for sequence variants that may have affected survival or susceptibility to the etiologic agent (Yersinia pestis).2 Third, mass mortality might alter the local gene pools through its impact on subsequent migration patterns. We explored these factors using the Norwegian city of Trondheim as a model, by sequencing 54 genomes spanning three time periods: (1) prior to the plague striking Trondheim in 1,349 CE, (2) the 17th–19th century, and (3) the present. We find that the pandemic period shaped the gene pool by reducing long distance immigration, in particular from the British Isles, and inducing a bottleneck that reduced genetic diversity. Although we also observe an excess of large FST values at multiple loci in the genome, these are shaped by reference biases introduced by mapping our relatively low genome coverage degraded DNA to the reference genome. This implies that attempts to detect selection using ancient DNA (aDNA) datasets that vary by read length and depth of sequencing coverage may be particularly challenging until methods have been developed to account for the impact of differential reference bias on test statistics.publishedVersio

A homozygous loss-of-function mutation leading to CYBC1 deficiency causes chronic granulomatous disease

Publisher's version (útgefin grein) Publisher’s note: Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.Mutations in genes encoding subunits of the phagocyte NADPH oxidase complex are recognized to cause chronic granulomatous disease (CGD), a severe primary immunodeficiency. Here we describe how deficiency of CYBC1, a previously uncharacterized protein in humans (C17orf62), leads to reduced expression of NADPH oxidase’s main subunit (gp91phox) and results in CGD. Analyzing two brothers diagnosed with CGD we identify a homozygous loss-of-function mutation, p.Tyr2Ter, in CYBC1. Imputation of p.Tyr2Ter into 155K chipgenotyped Icelanders reveals six additional homozygotes, all with signs of CGD, manifesting as colitis, rare infections, or a severely impaired PMA-induced neutrophil oxidative burst. Homozygosity for p.Tyr2Ter consequently associates with inflammatory bowel disease (IBD) in Iceland (P = 8.3 × 10−8; OR = 67.6), as well as reduced height (P = 3.3 × 10−4; −8.5 cm). Overall, we find that CYBC1 deficiency results in CGD characterized by colitis and a distinct profile of infections indicative of macrophage dysfunction.We wish to thank the family of the two probands, as well as all the other individuals who participated in the study and whose contribution made this work possible.Peer Reviewe

Physical and cognitive impact following SARS-CoV-2 infection in a large population-based case-control study

© 2023. The Author(s).BACKGROUND: Persistent symptoms are common after SARS-CoV-2 infection but correlation with objective measures is unclear. METHODS: We invited all 3098 adults who tested SARS-CoV-2 positive in Iceland before October 2020 to the deCODE Health Study. We compared multiple symptoms and physical measures between 1706 Icelanders with confirmed prior infection (cases) who participated, and 619 contemporary and 13,779 historical controls. Cases participated in the study 5-18 months after infection. RESULTS: Here we report that 41 of 88 symptoms are associated with prior infection, most significantly disturbed smell and taste, memory disturbance, and dyspnea. Measured objectively, cases had poorer smell and taste results, less grip strength, and poorer memory recall. Differences in grip strength and memory recall were small. No other objective measure associated with prior infection including heart rate, blood pressure, postural orthostatic tachycardia, oxygen saturation, exercise tolerance, hearing, and traditional inflammatory, cardiac, liver, and kidney blood biomarkers. There was no evidence of more anxiety or depression among cases. We estimate the prevalence of long Covid to be 7% at a median of 8 months after infection. CONCLUSIONS: We confirm that diverse symptoms are common months after SARS-CoV-2 infection but find few differences between cases and controls in objective parameters measured. These discrepancies between symptoms and physical measures suggest a more complicated contribution to symptoms related to prior infection than is captured with conventional tests. Traditional clinical assessment is not expected to be particularly informative in relating symptoms to a past SARS-CoV-2 infection.Peer reviewe

Chitosan leads to downregulation of YKL-40 and inflammasome activation in human macrophages.

To access publisher's full text version of this article click on the hyperlink at the bottom of the pageChitosan, the deacetylated derivative of chitin, is used as biomaterial in diverse settings. It is also found on pathogens and can be proinflammatory. Shorter derivatives of chitosan can be generated chemically or enzymatically, chitosan oligosaccharides (ChOS). There is variation in the chemical composition of ChOS, including size distribution, but in general, they have been described as inert or anti-inflammatory. Active human chitinases can cleave chitin and chitosan, while inactive chitinases bind both but do not cleave. Both active and inactive chitinases have important roles in the immune response. The inactive chitinase YKL-40 is expressed highly during inflammation and has been proposed as a marker of poor prognosis. YKL-40 acts as a negative regulator of the inflammasome and as a positive regulator of angiogenesis. Levels of YKL-40 can therefore regulate levels of inflammation, the extent of angiogenesis, and the process of inflammation resolution. This study shows that chitosan leads to reduced secretion of YKL-40 by primary human macrophages and that this is concomitant with inflammasome activation. This was most pronounced with a highly deacetylated ChOS. No effect on the secretion of the active chitinase Chit-1 was detected. Smaller and more acetylated ChOS did not affect YKL-40 levels nor inflammasome activation. We conclude that this effect on the levels of YKL-40 is a part of the proinflammatory mechanisms of chitosan and its derivatives. © 2015 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 103A: 2778-2785, 2015.Landspitali University Hospital Research Fund Icelandic Student Innovation Fund 132341009

Survival of patients with alcohol use disorders discharged from an emergency department: a population-based cohort study.

To access publisher's full text version of this article, please click on the hyperlink in Additional Links field or click on the hyperlink at the top of the page marked Files. This article is open access.The aim was to study the cause-specific mortality of users of the emergency department (ED) who received a diagnosis of alcohol use disorder (AUD) in comparison with mortality of other users of the department.A population-based prospective cohort study.All patients aged 18 years and above who were subsequently discharged home from the ED during the years 2002-2008. A total of 107,237 patients were followed by record linkage to a nationwide cause-of-death registry: 1210 patients with AUD as the main discharge diagnosis and 106,027 patients in the comparison group. HR and 95% CIs were calculated.ED at Landspitali-the National University Hospital of Iceland, Reykjavik, Iceland. The hospital offers tertiary care and is the number one trauma centre and community hospital for the greater Reykjavik area. According to the population registry, 78% of the inhabitants of the area attended the ED during the study period.72 patients died in the AUD group and 4807 in the comparison group. The adjusted HR for all causes of death was 1.91 (95% CI 1.51 to 2.42). The HR for AUDs was 47.68 (95% CI 11.56 to 196.59) while for alcohol liver disease the HR was 19.06 (95% CI 6.07 to 59.87). The HR was also elevated for diseases of the circulatory system: HR 2.52 (95% CI 1.73 to 3.68); accidental poisoning: HR=13.64, (95% CI 3.98 to 46.73); suicide: HR=2.72 (95% CI 1.08 to 6.83); and event of undetermined intent: HR=10.89 (95% CI 4.53 to 26.16).AUD as the discharge diagnosis at the ED, among patients who were not admitted to a hospital ward but discharged home, predicts increased mortality. As the results conclusively show the vulnerability of these patients, one can question whether their needs are adequately met at the ED.Landspitali—the National University Hospital Research Fund, Icelandic Nurse’s Association Research Fund/311055-2249; e University of Iceland Research Fund/1238-123368

Glucocorticoid dexamethasone down-regulates basal and vitamin D3 induced cathelicidin expression in human monocytes and bronchial epithelial cell line.

To access publisher's full text version of this article click on the hyperlink at the bottom of the pageGlucocorticoids (GCs) have been extensively used as the mainstream treatment for chronic inflammatory disorders. The persistent use of steroids in the past decades and the association with secondary infections warrants for detailed investigation into their effects on the innate immune system and the therapeutic outcome. In this study, we analyse the effect of GCs on antimicrobial polypeptide (AMP) expression. We hypothesize that GC related side effects, including secondary infections are a result of compromised innate immune responses. Here, we show that treatment with dexamethasone (Dex) inhibits basal mRNA expression of the following AMPs; human cathelicidin, human beta defensin 1, lysozyme and secretory leukocyte peptidase 1 in the THP-1 monocytic cell-line (THP-1 monocytes). Furthermore, pre-treatment with Dex inhibits vitamin D3 induced cathelicidin expression in THP-1 monocytes, primary monocytes and in the human bronchial epithelial cell line BCi NS 1.1. We also demonstrate that treatment with the glucocorticoid receptor (GR) inhibitor RU486 counteracts Dex mediated down-regulation of basal and vitamin D3 induced cathelicidin expression in THP-1 monocytes. Moreover, we confirmed the anti-inflammatory effect of Dex. Pre-treatment with Dex inhibits dsRNA mimic poly IC induction of the inflammatory chemokine IP10 (CXCL10) and cytokine IL1B mRNA expression in THP-1 monocytes. These results suggest that GCs inhibit innate immune responses, in addition to exerting beneficial anti-inflammatory effects.Icelandic Centre for Research (RANNIS) 130202-052 University of Iceland Research Fund Swedish Foundation for Strategic Research (SSF) RBd08-0014 Swedish Heart-Lung Foundation 2013-0366 Swedish Research Council K2014-67X-11217-20-3 Wenner-Gren Foundatio

Images and objects active methodology toolkit 2 : personal consumption and climate change

The Partnership for Education and Research about Responsible Living (PERL) is a partnership of educators, researchers and practitioners from more than 120 institutions in over 50 countries. The partners of PERL include universities, research institutes, international organisations, national and local civil society organisations and some small and medium enterprises. PERL is based on six years of work previously carried out by the Consumer Citizenship Network (CCN). PERL aims to advance education for responsible living by focusing on consumer citizenship, education for sustainable consumption, social innovation and sustainable lifestyles.peer-reviewe