Viðhorf barna til hreyfingar

Neðst á síðunni er hægt að nálgast greinina í heild sinni með því að smella á hlekkinn View/OpenPhysical activity among children seems to be diminishing around the world. This can be traced to modern life which is characterized by sedentary lifestyles, produced by a technological development. The World Health Organisation has identified children’s inactivity as a major public health problem (WHO, 2002). To be able to increase physical activity there needs to be more understanding of the ways physical activity affects children’s lives. The aim of the study was to explore children’s and parents’ views and beliefs about physical activity and health. This was done by identifying the factors that influence physical activity among children through examining children’s and parents’ own accounts of the place of physical (in)activity in children’s live. Qualitative research method was thought to be appropriate to get this information using focus groups, analysed by grounded theory. Literature reveals an extensive amount of research on the effects of physical activity on children. These studies however are mostly done on children and not with children. As a result there is a shortage of their perspectives. This study seeks to fill a gap in this knowledge by focusing on children’s and parent experience and beliefs. The findings of this study suggest a holistic approach to physical activity. Children want to be active and need to be given the opportunity to do so. Collaboration from all concerning parties, including children, is needed to create environments that enable and encourage physical activity. Increasing physical activity in childhood by establishing a safe and stimulating environment could be seen as an important factor in public health strategy.Hreyfingarleysi meðal barna er vaxandi áhyggjuefni sem og hugsanleg áhrif þess á lýðheilsu þjóða. Alþjóða Heilbrigðisstofnunin (WHO 2002) áætlar að minna en einn þriðji ungs fólks fái þá hreyfingu sem þarf til að halda góðri heilsu í nútíð og til framtíðar. Til að snúa þessari þróun við hafa yfirvöld víða um heim lagt mikla áherslu á að grípa til aðgerða í þeim tilgangi að auka hreyfingu meðal barna. Hreyfingarleysi barna hefur verið mikið til umræðu á Vesturlöndum og fjöldi rannsókna framkvæmdar til að varpa ljósi á vandann. Þessar rannsóknir sýna ýmsar hliðar á ástæðunum og hugsanlegum afleiðingum hreyfingarleysis. Rannsóknirnar hafa að mestu verið gerðar á börnum en ekki með þeim og því hafa skoðanir og reynsla barna af ástæðum/afleiðingum hreyfingarleysis lítt verið skoðaðar. Afleiðingar þessa eru að ekki er nægjanleg þekking á skoðunum barna á hreyfingu en rannsóknir með börnum hljóta þó að vera grundvöllur þess að við öðlumst frekari skilning á þörfum þeirra og meiningum. Upplýsingarnar sem þannig fengjust væri svo hægt að nota við stefnumótun og íhlutanir til að auka hreyfingu meðal barna

Interactions between innate immune effectors and multidrug resistant bacteria

Antibiotic resistance is an increasingly difficult problem in the clinic, where conventional antibiotics are failing, and new alternative solutions are in high demand. Infections caused by Gram-negative bacteria with multi drug resistance (MDR) mechanisms are increasing globally, and treatment options are limited. Plasmids encoding β-lactamases spread easily between bacteria, and the overuse of antibiotics select for MDR strains. β-lactamases are either serine- β-lactamases that are inhibited by certain β-lactamase inhibitors, and metallo-β-lactamases (MBLs), which are more difficult to inhibit with drugs. The current approach to fight MDR pathogens has mainly focused on finding β-lactamase inhibitors to use in combination with conventional antibiotics in the clinic. The overall aim of this thesis was to study the role of the cellular micro-environment and the importance of the innate immune system for antibiotic resistant bacterial infections. In Paper I we hypothesized that human cells secreted factors that could impair β-lactamase function and thus restore antibiotic susceptibility in resistant bacterial isolates. We found that thiols produced by the cells acted as zinc chelators that inhibited the degradation of cephalosporin antibiotics in VIM-1 producing K. pneumoniae. Notably, free thiols in urine samples had the same effect, suggesting that the environment at the site of infection can be highly important for antibiotic susceptibility and possibly also for the effect of antibiotic treatment in a clinical situation. In Paper II, we hypothesized that induction of innate effector molecules would reduce intracellular growth of MDR K. pneumoniae and exert synergistic effects with conventional antibiotics. We tested this by infecting human macrophages with MDR K. pneumoniae. Notably, induction of innate immunity in these cells resulted in improved intracellular killing of MDR K. pneumoniae. The inducers were combined with traditional antibiotics, which resulted in an additive killing effect. The data suggests that inducing innate immune effectors can be an effective alternative or addition to conventional treatments in infections caused by MDR K. pneumoniae. Finally, in Paper III, we tested the hypothesis that ESBL E. coli would be more susceptible to innate effectors compared to non-ESBL isolates. The ESBL producing isolates had lower survival in serum and whole blood than non-ESBL isolates, suggesting a biological cost for resistant isolates. In vivo studies with zebrafish embryos showed that the non-ESBL isolates killed the embryos more efficiently than ESBL isolates. The biological cost was not related to the ESBL plasmid per se as shown by experiments where the ESBL plasmid was transferred from a clinical isolate to a neutral background in non-resistant E. coli. Together, this thesis has highlighted the importance of considering the micro-environment at the site of infection, which may determine the effect of antibiotics. Next, I have shown that induction of innate immune effectors could be an alternative or additive treatment option for infections caused by MDR K. pneumoniae. Finally, I present data showing that ESBL E. coli are more susceptible to innate effectors than non-ESBL E. coli

The bright and the dark side of myelin plasticity: Neuron-glial interactions in health and disease.

Neuron-glial interactions shape neural circuit establishment, refinement and function. One of the key neuron-glial interactions takes place between axons and oligodendroglial precursor cells. Interactions between neurons and oligodendrocyte precursor cells (OPCs) promote OPC proliferation, generation of new oligodendrocytes and myelination, shaping myelin development and ongoing adaptive myelin plasticity in the brain. Communication between neurons and OPCs can be broadly divided into paracrine and synaptic mechanisms. Following the Nobel mini-symposium "The Dark Side of the Brain" in late 2019 at the Karolinska Institutet, this mini-review will focus on the bright and dark sides of neuron-glial interactions and discuss paracrine and synaptic interactions between neurons and OPCs and their malignant counterparts

White Matter Plasticity Keeps the Brain in Tune: Axons Conduct While Glia Wrap.

Precise timing of neuronal inputs is crucial for brain circuit function and development, where it contributes critically to experience-dependent plasticity. Myelination therefore provides an important adaptation mechanism for vertebrate circuits. Despite its importance to circuit activity, the interplay between neuronal activity and myelination has yet to be fully elucidated. In recent years, significant attention has been devoted to uncovering and explaining the phenomenon of white matter (WM) plasticity. Here, we summarize some of the critical evidence for modulation of the WM by neuronal activity, ranging from human diffusion tensor imaging (DTI) studies to experiments in animal models. These experiments reveal activity-dependent changes in the differentiation and proliferation of the oligodendrocyte lineage, and in the critical properties of the myelin sheaths. We discuss the implications of such changes for synaptic function and plasticity, and present the underlying mechanisms of neuron-glia communication, with a focus on glutamatergic signaling and the axomyelinic synapse. Finally, we examine evidence that myelin plasticity may be subject to critical periods. Taken together, the present review aims to provide insights into myelination in the context of brain circuit formation and function, emphasizing the bidirectional interplay between neurons and myelinating glial cells to better inform future investigations of nervous system plasticity

Neuronal activity-dependent myelin repair after stroke.

Brain tissue undergoes substantial activity-dependent reorganisation after stroke due to neuronal plasticity, leading to partial functional recovery in patients. Concurrent myelin repair is crucial for proper neuronal network function and reorganisation. Myelin repair after stroke might occur as myelin plasticity or as remyelination through the recruitment and differentiation of oligodendrocyte precursor cells (OPCs), which become myelin-forming oligodendrocytes (OLs). These two processes might share a similar guiding mechanism, which is postulated to depend on neuronal activity and glutamate signaling to OPCs. However, with ageing, the ability of OPCs to differentiate into myelinating OLs decreases due to changes in their ion channel and neurotransmitter receptor expression profile, rendering them less sensitive to neuronal activity. Because of their unique ability to replace damaged OLs, OPCs represent a potential therapeutic target for myelin repair in the context of stroke

A Matter of State: Diversity in Oligodendrocyte Lineage Cells.

Oligodendrocyte precursor cells (OPCs) give rise to oligodendrocytes which myelinate axons in the central nervous system. Although classically thought to be a homogeneous population, OPCs are reported to have different developmental origins and display regional and temporal diversity in their transcriptome, response to growth factors, and physiological properties. Similarly, evidence is accumulating that myelinating oligodendrocytes display transcriptional heterogeneity. Analyzing this reported heterogeneity suggests that OPCs, and perhaps also myelinating oligodendrocytes, may exist in different functional cell states. Here, we review the evidence indicating that OPCs and oligodendrocytes are diverse, and we discuss the implications of functional OPC states for myelination in the adult brain and for myelin repair

The case of Fish skin, a historical material assimilated as an innovative sustainable material for fashion.

This chapter is a study of northern indigenous fish skin heritage and builds connections among anthropology, ethnography, and material culture to address current global issues of fashion sustainability. It critically examines the historical application of the fish-skin craft and investigates the relationship of Arctic indigenous people with fish and the environment, fish skin fashion in the Arctic, the importance of women and fish skin art, the disappearance of the craft. The case study of the fashion designer John Galliano’s use of fish leather for garments in his Autumn/Winter 2002 collection is presented, situating the use of fish leather within the context of the luxury industry

White Matter Plasticity Keeps the Brain in Tune: Axons Conduct While Glia Wrap

Precise timing of neuronal inputs is crucial for brain circuit function and development, where it contributes critically to experience-dependent plasticity. Myelination therefore provides an important adaptation mechanism for vertebrate circuits. Despite its importance to circuit activity, the interplay between neuronal activity and myelination has yet to be fully elucidated. In recent years, significant attention has been devoted to uncovering and explaining the phenomenon of white matter (WM) plasticity. Here, we summarize some of the critical evidence for modulation of the WM by neuronal activity, ranging from human diffusion tensor imaging (DTI) studies to experiments in animal models. These experiments reveal activity-dependent changes in the differentiation and proliferation of the oligodendrocyte lineage, and in the critical properties of the myelin sheaths. We discuss the implications of such changes for synaptic function and plasticity, and present the underlying mechanisms of neuron–glia communication, with a focus on glutamatergic signaling and the axomyelinic synapse. Finally, we examine evidence that myelin plasticity may be subject to critical periods. Taken together, the present review aims to provide insights into myelination in the context of brain circuit formation and function, emphasizing the bidirectional interplay between neurons and myelinating glial cells to better inform future investigations of nervous system plasticity