Mänskliga rättigheter i gymnasiet : vad är det?

I uppsatsen analyseras fyra skolböcker som är avsedda för gymnasieskolans sam- hällskapliga utbildningar. Rebecca Adamis artikel, Re-Thinking Relations in Human Rights Education har fungerat som teori men också som verktyg eller nyckel i analysarbetet. Genom att använda Adamis kritik som grundar sig i hur västerländsk kultur prioriteras och normaliseras inom ämnet Human Right Education (HRE) och hur etnicitet, religion och politisk situation från andra kulturer framställs eller nedprioriteras. Arbete har visat hur FN:s deklaration om de mänskliga rättigheterna och konventionen om medborgerliga och politiska rättigheter samt konventionen om ekonomiska so- ciala och kulturella rättigheter får en stor del i författarnas berättelse om de mänskliga rättigheterna. Bristen på kritik och alternativ som problematiserar ämnet gör möjligheten för att inkludera eleverna i ämnet begränsat. En klassisk bild utav de mänskliga rättigheterna presenteras i böckerna trots att vi idag känner till brister i det system som byggdes upp efter andra världskriget. Human Rights Education har en roll att inte bara utbilda om utan även genom och viktigast av allt för de mänskliga rättigheterna. Genom att inkludera eleverna i berättelsen om de mänskliga rättigheterna så skapar vi ett bredare synsätt om ämnet. Hjälper skolböckerna våra lärare att visa för och nackdelar med vårt system vi använder idag och öppnar upp för dialog där elevernas erfarenheter och kunskaper tas om hand om? Är ämnet uppbyggt så att eleverna kan känna igen sig eller presenteras en bild av ett ämne som känns politiskt, internationellt och abstrakt

Hybridized Isogeometric Method for Elliptic Problems on CAD Surfaces with Gaps

We develop a method for solving elliptic partial differential equations on surfaces described by CAD patches that may have gaps/overlaps. The method is based on hybridization using a three-dimensional mesh that covers the gap/overlap between patches. Thus, the hybrid variable is defined on a three-dimensional mesh, and we need to add appropriate normal stabilization to obtain an accurate solution, which we show can be done by adding a suitable term to the weak form. In practical applications, the hybrid mesh may be conveniently constructed using an octree to efficiently compute the necessary geometric information. We prove error estimates and present several numerical examples illustrating the application of the method to different problems, including a realistic CAD model

Влияние национального менталитета на инновационную политику Республики Беларусь

Материалы VII междунар. науч. конф., 26-27 мая 2011 г

Klotho controls the brain-immune system interface in the choroid plexus.

Located within the brain's ventricles, the choroid plexus produces cerebrospinal fluid and forms an important barrier between the central nervous system and the blood. For unknown reasons, the choroid plexus produces high levels of the protein klotho. Here, we show that these levels naturally decline with aging. Depleting klotho selectively from the choroid plexus via targeted viral vector-induced knockout in Klotho flox/flox mice increased the expression of multiple proinflammatory factors and triggered macrophage infiltration of this structure in young mice, simulating changes in unmanipulated old mice. Wild-type mice infected with the same Cre recombinase-expressing virus did not show such alterations. Experimental depletion of klotho from the choroid plexus enhanced microglial activation in the hippocampus after peripheral injection of mice with lipopolysaccharide. In primary cultures, klotho suppressed thioredoxin-interacting protein-dependent activation of the NLRP3 inflammasome in macrophages by enhancing fibroblast growth factor 23 signaling. We conclude that klotho functions as a gatekeeper at the interface between the brain and immune system in the choroid plexus. Klotho depletion in aging or disease may weaken this barrier and promote immune-mediated neuropathogenesis

Bomapin is a redox-sensitive nuclear serpin that affects responsiveness of myeloid progenitor cells to growth environment

<p>Abstract</p> <p>Background</p> <p>Haematopoiesis is a process of formation of mature blood cells from hematopoietic progenitors in bone marrow. Haematopoietic progenitors are stimulated by growth factors and cytokines to proliferate and differentiate, and they die via apoptosis when these factors are depleted. An aberrant response to growth environment may lead to haematological disorders. Bomapin (serpinb10) is a hematopoietic- and myeloid leukaemia-specific protease inhibitor with unknown function.</p> <p>Results</p> <p>We found that the majority of naturally expressed bomapin was located in the nucleus. Both the natural and recombinant bomapin had a disulfide bond which linked the only two bomapin cysteines: one located in the CD-loop and the other near the C-terminus. Computer modelling showed that the cysteines are distant in the reduced bomapin, but can easily be disulfide-linked without distortion of the overall bomapin structure. Low-level ectopic expression of bomapin in bomapin-deficient K562 cells resulted in about 90% increased cell proliferation under normal growth conditions. On the other hand, antisense-downregulation of natural bomapin in U937 cells resulted in a decreased cell proliferation. Bomapin C395S mutant, representing the reduced form of the serpin, had no effect on cell proliferation, suggesting that the disulfide bond-linked conformation of bomapin is biologically important. The bomapin-dependent effect was specific for myeloid cells, since ectopic expression of the serpin in HT1080 cells did not change cell proliferation. In contrast to the survival-promoting activity of bomapin in cells cultured under optimal growth conditions, bomapin enhanced cell apoptosis following growth factor withdrawal.</p> <p>Conclusions</p> <p>We propose that bomapin is a redox-sensitive nuclear serpin that augments proliferation or apoptosis of leukaemia cells, depending on growth factors availability.</p

Loss of LRPPRC causes ATP synthase deficiency

Defects of the oxidative phosphorylation system, in particular of cytochrome-c oxidase (COX, respiratory chain complex IV), are common causes of Leigh syndrome (LS), which is a rare neurodegenerative disorder with severe progressive neurological symptoms that usually present during infancy or early childhood. The COX-deficient form of LS is commonly caused by mutations in genes encoding COX assembly factors, e.g. SURF1, SCO1, SCO2 or COX10. However, other mutations affecting genes that encode proteins not directly involved in COX assembly can also cause LS. The leucine-rich pentatricopeptide repeat containing protein (LRPPRC) regulates mRNA stability, polyadenylation and coordinates mitochondrial translation. In humans, mutations in Lrpprc cause the French Canadian type of LS. Despite the finding that LRPPRC deficiency affects the stability of most mitochondrial mRNAs, its pathophysiological effect has mainly been attributed to COX deficiency. Surprisingly, we show here that the impaired mitochondrial respiration and reduced ATP production observed in Lrpprc conditional knockout mouse hearts is caused by an ATP synthase deficiency. Furthermore, the appearance of inactive subassembled ATP synthase complexes causes hyperpolarization and increases mitochondrial reactive oxygen species production. Our findings shed important new light on the bioenergetic consequences of the loss of LRPPRC in cardiac mitochondria