Å mene noe annet enn flertallet - Historiene på siden av de rådene diskursene under Covid-19 pandemien

Denne masteroppgaven handler om hvordan det kunne være å ha andre, motstridende meninger enn de rådende diskursene under Covid-19 pandemien. Fire ressurssterke kvinner gir et innblikk i hvilken påvirkning dette hadde for deres sosiale relasjoner, hvordan de opplevde autonomi i eget liv og hvordan situasjonen innvirket på deres selv. Problemstillingen og forskningsspørsmålene ble inspirert av den tilsynelatende ensidige forståelsen og håndteringen av pandemien under det første halvannet året. Diskursanalyse brukes for å analysere data, og tre overordnede diskurser trer frem: ytringsfrihet i Norge, å bestemme over egen helse og relasjoners betydning for individer. I temaet om ytringsfrihet i Norge reflekterer deltagerne rundt opplevelsen av å ha en annen mening enn flertallet i samfunnet og hvordan de opplevde en begrensning i ytringsfriheten. Diskusjonen tar for seg konsekvensene deltagerne opplever i samfunnet som følge av sine motstridende meninger, hvordan språklige virkemidler brukes strategisk i kommunikasjonen med leseren og påvirkning av deltagernes selv. Under temaet om retten til å bestemme over egen helse fremkommer det dilemmaer og motsetninger mellom autonomi til å ta valg for egen helse eller etterfølge krav og forventninger fra samfunnet. Det diskuteres rundt bevarelsen av selvrespekten, tillit til myndighetenes håndtering av pandemien og hvordan maktens mekanismer innvirker på samfunnet. I temaet om relasjoners betydning for individet forteller deltagerne historier om hvordan deres ulike relasjoner blir affisert ved at de konstruerer andre verdensbilder enn flertallet. Det er både positive og negative konsekvenser for deltagerne. Påvirkningen i relasjonene drøftes ved hjelp av eksistensielle begreper om tro, håp, forsoning, tilgivelse og dialog. En del av diskusjonen løftes inn i konteksten av terapirommet for å vise relevansen til det systemiske terapifeltet. Viktigheten av terapeutens selvrefleksive bevissthet trer her tydelig frem

Quantitative proteomics analysis of zebrafish exposed to sub-lethal dosages of β-methyl-amino-L-alanine (BMAA)

The non-protein amino acid β-methylamino-L-alanine (BMAA) is a neurotoxin present in microalgae and shown to accumulate in the food web. BMAA has been linked to the complex neurodegenerative disorder of Guam and to increased incidents sporadic ALS. Two main neurotoxic routes are suggested; an excitotoxic by acting as an agonist towards glutamate receptors and a metabolic by misincorporating into cellular proteins. We have used zebrafish, an increasingly used model for neurodegenerative diseases, to further identify signaling components involved in BMAA-induced toxicity. Zebrafish embryos were exposed to sub-lethal dosages of BMAA and a label-free proteomics analysis was conducted on larvae 4 days post fertilization. The exposed larvae showed no developmental abnormalities, but a reduced heart rate and increased expression of GSK3 isoforms. Search towards a reviewed database containing 2968 entries identified 480 proteins. Only 17 of these were regulated 2-fold or more in the exposed larvae. Seven of these proteins could be associated to glutamate receptor signaling and recycling. The remaining nine have all been linked to disturbance in protein homeostasis, reactive oxygen species (ROS) development or neuronal cell death. We also found that BMAA influenced the endocannabinoid system by up-regulation of fatty acid amide hydrolase (FAAH) and that FAAH inhibitor URB597 reduced the BMAA effect on heart rate and GSK3 expression.publishedVersio

Glial contribution to excitatory and inhibitory synapse loss in neurodegeneration

Synapse loss is an early feature shared by many neurodegenerative diseases, and it represents the major correlate of cognitive impairment. Recent studies reveal that microglia and astrocytes play a major role in synapse elimination, contributing to network dysfunction associated with neurodegeneration. Excitatory and inhibitory activity can be affected by glia-mediated synapse loss, resulting in imbalanced synaptic transmission and subsequent synaptic dysfunction. Here, we review the recent literature on the contribution of glia to excitatory/inhibitory imbalance, in the context of the most common neurodegenerative disorders. A better understanding of the mechanisms underlying pathological synapse loss will be instrumental to design targeted therapeutic interventions, taking in account the emerging roles of microglia and astrocytes in synapse remodeling

How can nurses through communication help children in grief after a parental suicide?

Sjukepleie, Bachelorstudium Sk152 2015Forskning viser at selvmords-etterlatte barn kan stå overfor langsiktige problemer, både følelsesmessig og sosialt. Tidlig identifisering og terapeutisk intervensjon er avgjørende for å hindre negative helseeffekter. Et viktig fokus er på hvilken måte kommunikasjon kan hjelpe barn til å mestre det de har opplevd. Selv om det er svært vanskelig for barn og miste en forelder i selvmord, er det likevel ingen «livstidsdom». Ved god omsorg og støtte fra voksne omsorgspersoner og profesjonelle hjelpere, vil de aller fleste barn takle det at mor eller far dør, også ved selvmord. Det viktigste i møte med denne pasientgruppen er åpenhet, trygghet og alderstilpasset informasjon

Algal Toxin Azaspiracid-1 Induces Early Neuronal Differentiation and Alters Peripherin Isoform Stoichiometry

Azaspiracid-1 is an algal toxin that accumulates in edible mussels, and ingestion may result in human illness as manifested by vomiting and diarrhoea. When injected into mice, it causes neurotoxicological symptoms and death. Although it is well known that azaspiracid-1 is toxic to most cells and cell lines, little is known about its biological target(s). A rat PC12 cell line, commonly used as a model for the peripheral nervous system, was used to study the neurotoxicological effects of azaspiracid-1. Azaspiracid-1 induced differentiation-related morphological changes followed by a latter cell death. The differentiated phenotype showed peripherin-labelled neurite-like processes simultaneously as a specific isoform of peripherin was down-regulated. The precise mechanism behind this down-regulation remains uncertain. However, this study provides new insights into the neurological effects of azaspiracid-1 and into the biological significance of specific isoforms of peripherin

Reintroduction of dj-1 in müller cells inhibits retinal degeneration in the dj-1 deficient retina

The eye is continuously under oxidative stress due to high metabolic activity and reactive oxygen species generated by daily light exposure. The redox-sensitive protein DJ-1 has proven to be essential in order to protect retina and retinal pigment epithelium (RPE) from oxidative-stress-induced degeneration. Here, we analyzed the specific role of Müller cell DJ-1 in the adult zebrafish retina by re-establishing Müller-cell-specific DJ-1 expression in a DJ-1 knockout retina. Loss of DJ-1 resulted in an age-dependent retinal degeneration, including loss of cells in the ganglion cell layer, retinal thinning, photoreceptor disorganization and RPE cell dysfunction. The degenerative phenotype induced by the absence of DJ-1 was inhibited by solely expressing DJ-1 in Müller cells. The protective effect was dependent upon the cysteine-106 residue of DJ-1, which has been shown to be an oxidative sensor of DJ-1. In a label-free proteomics analysis of isolated retinas, we identified proteins differentially expressed after DJ-1 knockout, but with restored levels after Müller cell DJ-1 re-insertion

Reintroduction of dj-1 in müller cells inhibits retinal degeneration in the dj-1 deficient retina

The eye is continuously under oxidative stress due to high metabolic activity and reactive oxygen species generated by daily light exposure. The redox-sensitive protein DJ-1 has proven to be essential in order to protect retina and retinal pigment epithelium (RPE) from oxidative-stress-induced degeneration. Here, we analyzed the specific role of Müller cell DJ-1 in the adult zebrafish retina by re-establishing Müller-cell-specific DJ-1 expression in a DJ-1 knockout retina. Loss of DJ-1 resulted in an age-dependent retinal degeneration, including loss of cells in the ganglion cell layer, retinal thinning, photoreceptor disorganization and RPE cell dysfunction. The degenerative phenotype induced by the absence of DJ-1 was inhibited by solely expressing DJ-1 in Müller cells. The protective effect was dependent upon the cysteine-106 residue of DJ-1, which has been shown to be an oxidative sensor of DJ-1. In a label-free proteomics analysis of isolated retinas, we identified proteins differentially expressed after DJ-1 knockout, but with restored levels after Müller cell DJ-1 re-insertion. Our data show that Müller cell DJ-1 has a major role in protecting the retina from age-dependent oxidative stress

Reintroduction of dj-1 in müller cells inhibits retinal degeneration in the dj-1 deficient retina

The eye is continuously under oxidative stress due to high metabolic activity and reactive oxygen species generated by daily light exposure. The redox-sensitive protein DJ-1 has proven to be essential in order to protect retina and retinal pigment epithelium (RPE) from oxidative-stress-induced degeneration. Here, we analyzed the specific role of Müller cell DJ-1 in the adult zebrafish retina by re-establishing Müller-cell-specific DJ-1 expression in a DJ-1 knockout retina. Loss of DJ-1 resulted in an age-dependent retinal degeneration, including loss of cells in the ganglion cell layer, retinal thinning, photoreceptor disorganization and RPE cell dysfunction. The degenerative phenotype induced by the absence of DJ-1 was inhibited by solely expressing DJ-1 in Müller cells. The protective effect was dependent upon the cysteine-106 residue of DJ-1, which has been shown to be an oxidative sensor of DJ-1. In a label-free proteomics analysis of isolated retinas, we identified proteins differentially expressed after DJ-1 knockout, but with restored levels after Müller cell DJ-1 re-insertion.publishedVersio