No description available.

Diss. (sammanfattning) Stockholm : Karol. inst., 2005. / Härtill 5 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2004. / Härtill 5 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2004. / Härtill 4 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2006. / Härtill 4 uppsatser.

Thesis (DPhil)--Stellenbosch University, 2004. / ENGLISH ABSTRACT: This qualitative study comprised an in-depth investigation into the subjective - the explicitly human - experience of those suffering from Myalgic Encephalomyelitis (ME). I was, firstly, concerned with the nature and meaning of the social side of illness, that is, the sufferer's encounters with doctor, family member, friend and acquaintance alike. I was, secondly, set to develop greater insight into the essentially personal experience of being ill. I was able to conclude that, even amidst the inhumane presence of utter ignorance that permeate the very experience of ME, no ME sufferer is inevitably doomed a victim. They can always make a deliberate decision to have a say in their situation, in their own experience of their circumstances. They have the power of personal choice. Recommendations are, therefore, directed at expanding the potential extent and magnitude of this dynamic power. The substantive focus of my study was enriched by a deliberate concern with the methodological implications of my own intimate involvement within the research process. I was here primarily concerned with my personal contribution to the research process as well as the influence thereof on the research relationships developed and the research strategies chosen and applied. I could not but conclude that the understanding I explicate is, as all social science theory, essentially a human construction, developed by me, in my distinctly human capacity. Recommendations are, therefore, geared to sensitise all social researchers to their own contribution to the construction of that which is eventually presented (and taken) as truthful knowl~dge. In conclusion, I am thoroughly convinced that the experience of both illness and research is fundamentally human. This "humanness" cannot and should not be denied. Instead, I advocate a more deliberate focus on the human dimension of illness and research. Without such a focus, a more comprehensive understanding of either realm will continue to linger as but an elusive ideal. / AFRIKAANSE OPSOMMING: Hierdie kwalitatiewe studie is gebaseer op 'n in-diepte ondersoek gerig op die subjektiewe - die onteenseglik menslike - ervaring van diegene wat ly aan Myaligië Enkefalomiëlitis (ME). Ek was, eerstens, geïnteresseerd in die aard en betekenis van die sosiale dimensie van siekte, dit wil sê, die lyer se ervaring van sosiale kontak met dokters, gesinslede, vriende en kennisse. Ek was, tweedens, gerig op die ontwikkeling van 'n grondige insig in die uiters persoonlike ervaring van siek-wees. Ek het tot die gevolgtrekking gekom dat, selfs te midde van die onmenslike teenwoordigheid van blatante onkunde wat die ganse ervaring van ME kenmerk, geen ME lyer noodwendig tot 'n slagoffer-status gedoem is nie. Hulle kan altyd 'n doelbewuste besluit neem om 'n sê te hê in hul eie situasie, in hul eie ervaring van hul omstandighede. Hulle het die mag van persoonlike keuse. Aanbevelings is dus daarop gerig om die potentiële trefwydte en impak van hierdie dinamiese mag uit te brei. Die substantiewe dimensie van my studie is verryk deur 'n doelbewuste fokus op die metodologiese implikasies van my eie intieme betrokkenheid in die navorsingsproses. Ek was hoofsaaklik gemoeid met my persoonlike bydrae tot die navorsingsproses en die invloed daarvan op die ontwikkel van navorsingsverhoudings en die toepassing van gekose navorsingstrategieë. Hierdie fokus het gelei tot die besef dat die beskrywing wat ek aanbied, soos inderdaad alle sosiale teorie, essensieël 'n menslike konstruksie is, soos ontwikkel deur my, in my uitdruklik menslike kapasiteit. Aanbevelings is dus daarop gerig om alle sosiale navorsers te sensitiseer ten opsigte van hul eie bydrae tot die konstruksie van dit wat uiteindelik voorgestel (en geag) word as die waarheidsgetroue kennis. In slotsom, is ek oortuig dat die ervaring van beide siekte en navorsing fundamenteel menslik is. Hierdie "mensheid" kan en behoort nie ontken te word nie. Inteendeel, ek bepleit 'n doelbewuste fokus op die menslike dimensie van siekte en navorsing. Sonder só 'n fokus sal 'n meer diepgaande begrip van iedere area bloot 'n onbereikbare ideaal bly.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2005. / Härtill 6 uppsatser.

Thesis (Ph. D.)--Ohio State University, 2007. / Full text release at OhioLINK's ETD Center delayed at author's request

A subset of cyclophilins have been implicated in mechanisms of neuroinflammation and neurodegeneration that contributes to the pathogenesis of Multiple Sclerosis. Mitochondrial dysfunction leading to mitochondrial permeability transition plays a pivotal role in axonal damage and disease progression in Multiple Sclerosis. Cyclophilin D (CypD) is a crucial regulatory component of the mitochondrial permeability transition pore and it was demonstrated that the cyclophilin D knockout animals showed reduced experimental allergic encephalomyelitis (EAE) clinical disease severity and axonal injury. We investigated the effect of N-methyl-4-isoleucine-cyclosporin (NIM811), a non-immunosuppressive and non-selective cyclophilin inhibitor, on the course and severity of EAE. EAE mice treated with NIM811 showed a significant reduction in clinical disease severity compared to vehicle treated mice. FACS analysis performed with the dissociated thoracolumbar spine showed that NIM811 treatment was associated with a reduction in CNS macrophages but does not alter T-helper lineage frequencies. In addition, we demonstrated NIM811’s effect on crude mitochondrial fraction obtained from brain and liver homogenates of both wild type and CypD knockout mice in order to determine drug specificity. Benefits observed from the pharmacological inhibition of cyclophilin may lead to a novel MS therapy but NIM811’s exact mechanism of action has yet to be elucidated.

No description available.