Västerländsk mindfulnessmeditation har sina rötter i tusenårig buddhistisk tradition, främst genom vipassana- och zentraditionerna. Senaste tiden har mindfulness ökat i popularitet och blivit en accepterad klinisk metod i former som mindfulness based stress reduction. Möjligheten att undersöka dess effekter genom neurovetenskapliga metoder bidrar med intressant och viktig forskning om mänskligt välbefinnande. Dock har tidigare studier visat på bristande samstämmighet vad gäller resultat och metod. Uppsatsen är en litteraturstudie där det huvudsakliga syftet är att utifrån nyare studier undersöka de tydligaste effekterna på hjärnfunktion och struktur av långvarigt praktiserande av mindfulness utifrån vipassana- och zenmeditation. Uppsatsen syftar även till att redogöra för samstämmigheten i dessa nyare studier. Detta gäller resultat men också metod. Studierna tyder på minskad aktivitet i prefrontala cortex (PFC), posteriora cingulum cortex (PCC) och minskad aktivitet mellan PFC och regioner inom default mode network(DMN) som anteriora cingulum cortex (ACC). Studier visar även ökad aktivitet från parietala-occipitala området. Resultaten tyder på förbättrad kroppsmedvetenhet och ökad sensorisk klarhet, ökad förmåga till uppmärksamhetsreglering och inhibition av automatiska responser samt minskning av och ökad kontroll över det spontana flödet av tankar och en förändrad självuppfattning. Jag finner att resultaten var samstämmiga beträffande minskat involverande av frontala och parietala områden, samt svagare förbindelser mellan dessa (dlPFC-IPL, PFC-dACC). Gemensamt för studierna är också att mindfulnessmeditation tycks påverka DMN och områden kopplade till det självrefererande processandet. Det är dock inte klart hur predispositioner inverkat på resultaten och det är något för framtida forskning att klargöra.

<p>Denna litteraturöversikt jämför Sigmund Freuds drömteori med befintliga neurovetenskapliga forskningsfynd om drömmar för att finna likheter eller avvikelser dem emellan. Neuropsykoanalys är en tvärvetenskap som avser studera psykologiska fenomen med hjälp av neurovetenskaplig forskning och psykoanalytiska teorier. De båda fälten används för att belysa och stärka varandras fynd och postulat. Freuds teori som innebär att drömmar är önskeuppfyllelser och fyller funktionen av att vakta sömnen sammanfattas. Vidare sammanfattas neurovetenskapligt inriktad forskning som visar att drömmars karaktär styrs av hjärnstrukturers olika aktivitetsnivå och påverkan från signalsubstanser. Jämförelsen visar att neurovetenskapliga fynd talar för Freuds drömteori. Bland annat visas att system för behovsidentifiering och belöning är aktiva under sömn och att organismen skyddar sömn. Nervretningar aktiverar drömbildandet, kontrollfunktioner är hämmade under sömn och negativa emotioner präglar drömmar. Detta till trots kan teorin varken bekräftas eller dementeras med tillgänglig forskning.</p>

<p>Ultraviolet radiation (UV-R) is an environmental factor known to increase the risk of developing an irreversible opacification of the lens (cataract). Increased irradiance of UV-R to the earth because of depletion of stratospheric ozone is of current concern considering cataract formation. Detailed metabolic information from the cornea, lens and aqueous humour might give valuable knowledge on the biochcemical processes occurring in the eye after exposure to UV-R, and thereby a better understanding of the mechanisms by which UV-R induces cataractogenesis. The purpose of this thesis was to study metabolic effects of exposure to UV-R on the anterior part of the eye. Effects of UV-B (280-315 nm) and UV-A (315-400 nm) on the aqueous humour, cornea and the lens from animal models were investigated by ¹H nuclear magnetic resonance (NMR) spectroscopy. Since the lens is composed of functionally distinct anatomical compartments, with different metabolic activity, biochemical changes in various compartments of the lens were analyzed.</p><p>Application of NMR-based metabonomics was effective to analyze metabolic changes in the anterior part of the eye after exposure to UV-R. High-resolution (HR) magic angle spinning (MAS)¹H NMR spectroscopy provided high quality spectra from intact tissue of cornea and lens, and provided important information about metabolic alteration occurring in these tissues after exposure to UV-R. The results from this thesis show that in vivo UV-B radiation affects metabolism of the anterior compartments of the eye. Metabolic changes were observed in aqueous humour, cornea, lens and in the different compartments of the lens. The antioxidants, glutathione and ascorbate, several amino acids, high energetic phosphates, and compounds important for membrane building and osmoregulation were substantially altered after exposure to UV-B radiation. Several biochemical effects such as oxidation, membrane disruption, osmoregulatory problems, lipid peroxidation, problems with cellular signalling and impairment of growth and protein synthesis were suggested. After UV-A exposure, no observable metabolic alterations were found in the anterior part of the eye in the present animal models.</p>

<p>Recently discovered neuropeptides orexins (orexin-A and -B) act as endogenous ligands for G-protein-coupled receptors called OX₁ and OX₂ receptors. Our previous studies have established model systems for investigation of the pharmacology and signaling of these receptors in recombinant CHO cells. OX₁ receptor-expressing CHO cells were mainly utilized in this thesis.</p><p>Orexin-A and -B activate both OX₁ and OX₂ receptors. However, orexin-B is less potent in activating OX₁ receptors than orexin-A, whereas the peptides are equipotent on OX₂ receptors. We have performed mutagenesis on orexin-A to investigate the basis for this selectivity. We show that OX₂ receptor is generally less affected by the mutations and thus OX₂receptor appears to have less strict requirements for ligand binding, likely explaining the lack of difference in affinity/potency between orexin-A and orexin-B on OX₂ receptor.</p><p>The other studies focus on orexin receptor signaling. OX₁ receptors are shown to regulate adenylyl cyclase both in positive and negative manner, activate different MAP-kinases (ERK1/2 and p38) and induce cell death after long-lasting stimulation. Adenylyl cyclase regulation occurs likely through three different G-protein families, Gi, Gs and Gq. For ERK1/2, several downstream pathways, such as Ras, Src, PI3-kinase and protein kinase C (PKC) are implicated. OX₁ receptor-mediated activation of ERK is suggested to be cytoprotective whereas p38 MAP-kinase induces programmed cell death. </p><p>Three particularly interesting findings were made. Firstly, novel PKC δ (delta) is suggested to regulate adenylyl cyclase, whereas conventional and atypical PKCs are involved in activation of ERK. Secondly, adenylyl cyclase and ERK activation is fully dependent on extracellular Ca²⁺. Further experiments suggest that the previously discovered receptor-operated Ca²⁺ influx is not affecting the downstream effectors of orexin receptors but that it instead enables orexin receptors to couple to several signal cascades. Thirdly, upon inhibition of caspases, classical mediators of programmed cell death, OX₁receptor-mediated cell death is not reversed, but instead the pathways to death are altered so de novo gene transcription is no longer required for cell death.</p>

<p>The bradykinin and neuropeptide Y (NPY) receptors belong to the superfamily of G-protein coupled receptors (GPCRs). The GPCRs form the largest class of therapeutic targets and it is therefore of great interest to investigate the pharmacological properties, functions and evolution of these receptors.</p><p>Bradykinin (BK) is a nonapeptide that contributes to inflammatory responses, mediates pain signals and influences blood pressure. The two bradykinin receptor subtypes B1 and B2 are well characterized in mammals, but have received little attention in non-mammals. This thesis describes the cloning and characterization of the first piscine bradykinin receptor, from the <i>Danio rerio</i> (zebrafish). Ligand-receptor interactions were measured as production of intracellular inositol phosphate. Zebrafish BK activated the receptor with highest potency (pEC₅₀=6.97±0.1) while mammalian BK was almost inactive. A complete alanine and D-amino acid scan of the BK peptide revealed important roles for receptor interaction for residues Gly4, Ser6, Pro7, Leu8 and Arg9. The receptor gene was mapped to chromosome 17 in the zebrafish genome in a region that shows conserved synteny to the human B1-B2 gene region on chromosome 14. The release of the zebrafish and pufferfish genomes enabled us to identify both B1 and B2 genes in <i>Danio rerio</i> and pufferfishes (<i>Takifugu rubripes</i> and <i>Tetraodon nigroviridis</i>) as well as the B1 gene in chicken. All of these species display conserved synteny of the gene region. Interestingly, the evolutionary rate is clearly greater for B1 than for B2. Kininogen, the precursor for bradykinin, is also located in a chromosome region with extensive conserved synteny.</p><p>Neuropeptide Y (NPY), peptide YY (PYY) and pancreatic polypeptide (PP) comprise a family of related peptides and are involved in a variety of neuronal and endocrine functions. Receptor subtypes Y6 and Y7 were cloned and pharmacologically characterized in chicken. The genes are located one megabase apart on chromosome 13 in a region with conserved synteny to human chromosome 5. Porcine PYY bound to chicken Y6 with a K_d of 0.80±0.36 nM and chicken Y7 with a K_d of 0.14±0.01 nM. The Y6 mRNA is expressed in hypothalamus, gastrointestinal tract and adipose tissue and may be involved in appetite regulation like other NPY receptors. Chicken Y7 mRNA was only detected in adrenal gland. These results may help explain why these receptors have lost function in humans.</p>

Recently discovered neuropeptides orexins (orexin-A and -B) act as endogenous ligands for G-protein-coupled receptors called OX1 and OX2 receptors. Our previous studies have established model systems for investigation of the pharmacology and signaling of these receptors in recombinant CHO cells. OX1 receptor-expressing CHO cells were mainly utilized in this thesis. Orexin-A and -B activate both OX1 and OX2 receptors. However, orexin-B is less potent in activating OX1 receptors than orexin-A, whereas the peptides are equipotent on OX2 receptors. We have performed mutagenesis on orexin-A to investigate the basis for this selectivity. We show that OX2 receptor is generally less affected by the mutations and thus OX2 receptor appears to have less strict requirements for ligand binding, likely explaining the lack of difference in affinity/potency between orexin-A and orexin-B on OX2 receptor. The other studies focus on orexin receptor signaling. OX1 receptors are shown to regulate adenylyl cyclase both in positive and negative manner, activate different MAP-kinases (ERK1/2 and p38) and induce cell death after long-lasting stimulation. Adenylyl cyclase regulation occurs likely through three different G-protein families, Gi, Gs and Gq. For ERK1/2, several downstream pathways, such as Ras, Src, PI3-kinase and protein kinase C (PKC) are implicated. OX1 receptor-mediated activation of ERK is suggested to be cytoprotective whereas p38 MAP-kinase induces programmed cell death. Three particularly interesting findings were made. Firstly, novel PKC δ (delta) is suggested to regulate adenylyl cyclase, whereas conventional and atypical PKCs are involved in activation of ERK. Secondly, adenylyl cyclase and ERK activation is fully dependent on extracellular Ca2+. Further experiments suggest that the previously discovered receptor-operated Ca2+ influx is not affecting the downstream effectors of orexin receptors but that it instead enables orexin receptors to couple to several signal cascades. Thirdly, upon inhibition of caspases, classical mediators of programmed cell death, OX1 receptor-mediated cell death is not reversed, but instead the pathways to death are altered so de novo gene transcription is no longer required for cell death.

The bradykinin and neuropeptide Y (NPY) receptors belong to the superfamily of G-protein coupled receptors (GPCRs). The GPCRs form the largest class of therapeutic targets and it is therefore of great interest to investigate the pharmacological properties, functions and evolution of these receptors. Bradykinin (BK) is a nonapeptide that contributes to inflammatory responses, mediates pain signals and influences blood pressure. The two bradykinin receptor subtypes B1 and B2 are well characterized in mammals, but have received little attention in non-mammals. This thesis describes the cloning and characterization of the first piscine bradykinin receptor, from the Danio rerio (zebrafish). Ligand-receptor interactions were measured as production of intracellular inositol phosphate. Zebrafish BK activated the receptor with highest potency (pEC50=6.97±0.1) while mammalian BK was almost inactive. A complete alanine and D-amino acid scan of the BK peptide revealed important roles for receptor interaction for residues Gly4, Ser6, Pro7, Leu8 and Arg9. The receptor gene was mapped to chromosome 17 in the zebrafish genome in a region that shows conserved synteny to the human B1-B2 gene region on chromosome 14. The release of the zebrafish and pufferfish genomes enabled us to identify both B1 and B2 genes in Danio rerio and pufferfishes (Takifugu rubripes and Tetraodon nigroviridis) as well as the B1 gene in chicken. All of these species display conserved synteny of the gene region. Interestingly, the evolutionary rate is clearly greater for B1 than for B2. Kininogen, the precursor for bradykinin, is also located in a chromosome region with extensive conserved synteny. Neuropeptide Y (NPY), peptide YY (PYY) and pancreatic polypeptide (PP) comprise a family of related peptides and are involved in a variety of neuronal and endocrine functions. Receptor subtypes Y6 and Y7 were cloned and pharmacologically characterized in chicken. The genes are located one megabase apart on chromosome 13 in a region with conserved synteny to human chromosome 5. Porcine PYY bound to chicken Y6 with a Kd of 0.80±0.36 nM and chicken Y7 with a Kd of 0.14±0.01 nM. The Y6 mRNA is expressed in hypothalamus, gastrointestinal tract and adipose tissue and may be involved in appetite regulation like other NPY receptors. Chicken Y7 mRNA was only detected in adrenal gland. These results may help explain why these receptors have lost function in humans.

Ultraviolet radiation (UV-R) is an environmental factor known to increase the risk of developing an irreversible opacification of the lens (cataract). Increased irradiance of UV-R to the earth because of depletion of stratospheric ozone is of current concern considering cataract formation. Detailed metabolic information from the cornea, lens and aqueous humour might give valuable knowledge on the biochcemical processes occurring in the eye after exposure to UV-R, and thereby a better understanding of the mechanisms by which UV-R induces cataractogenesis. The purpose of this thesis was to study metabolic effects of exposure to UV-R on the anterior part of the eye. Effects of UV-B (280-315 nm) and UV-A (315-400 nm) on the aqueous humour, cornea and the lens from animal models were investigated by 1H nuclear magnetic resonance (NMR) spectroscopy. Since the lens is composed of functionally distinct anatomical compartments, with different metabolic activity, biochemical changes in various compartments of the lens were analyzed. Application of NMR-based metabonomics was effective to analyze metabolic changes in the anterior part of the eye after exposure to UV-R. High-resolution (HR) magic angle spinning (MAS) 1H NMR spectroscopy provided high quality spectra from intact tissue of cornea and lens, and provided important information about metabolic alteration occurring in these tissues after exposure to UV-R. The results from this thesis show that in vivo UV-B radiation affects metabolism of the anterior compartments of the eye. Metabolic changes were observed in aqueous humour, cornea, lens and in the different compartments of the lens. The antioxidants, glutathione and ascorbate, several amino acids, high energetic phosphates, and compounds important for membrane building and osmoregulation were substantially altered after exposure to UV-B radiation. Several biochemical effects such as oxidation, membrane disruption, osmoregulatory problems, lipid peroxidation, problems with cellular signalling and impairment of growth and protein synthesis were suggested. After UV-A exposure, no observable metabolic alterations were found in the anterior part of the eye in the present animal models.

Denna litteraturöversikt jämför Sigmund Freuds drömteori med befintliga neurovetenskapliga forskningsfynd om drömmar för att finna likheter eller avvikelser dem emellan. Neuropsykoanalys är en tvärvetenskap som avser studera psykologiska fenomen med hjälp av neurovetenskaplig forskning och psykoanalytiska teorier. De båda fälten används för att belysa och stärka varandras fynd och postulat. Freuds teori som innebär att drömmar är önskeuppfyllelser och fyller funktionen av att vakta sömnen sammanfattas. Vidare sammanfattas neurovetenskapligt inriktad forskning som visar att drömmars karaktär styrs av hjärnstrukturers olika aktivitetsnivå och påverkan från signalsubstanser. Jämförelsen visar att neurovetenskapliga fynd talar för Freuds drömteori. Bland annat visas att system för behovsidentifiering och belöning är aktiva under sömn och att organismen skyddar sömn. Nervretningar aktiverar drömbildandet, kontrollfunktioner är hämmade under sömn och negativa emotioner präglar drömmar. Detta till trots kan teorin varken bekräftas eller dementeras med tillgänglig forskning.

I föreliggande studie har gymnasieelevers uppfattning om sin egen koncentrationsförmåga undersökts liksom vilka faktorer de upplever främjar/hämmar denna förmåga. Studien tar sin teoretiska utgångspunkt i den neurovetenskapliga forskningen och undersöker om elevernas uppfattningar har några möjliga förklaringar och överensstämmelser med denna relativt nya forskning. Eleverna gavs även möjlighet till metakognitiv reflektion kring huruvida de anser att den neurovetenskapliga forskningen skulle kunna stötta deras koncentration. En kvalitativ studie i form av en enkät och tre gruppintervjuer genomfördes i årskurs tre på ett studieförbe-redande program varpå resultaten analyserades fenomenografiskt och de tydligaste resultaten lyftes fram. Resultaten av studien visar på att det finns flertalet uppfattningar hos eleverna som skulle kunna förklaras med stöd av den neurovetenskapliga forskningen. Exempel på sådana uppfattningar är att avskärmning och lagom svåra uppgifter främjar koncentrationen medan sömnbrist och försök till att använda sociala medier på mobiltelefonen samtidigt som man studerar hämmar elevernas förmåga. Resultaten visar även att eleverna ser på koncentra-tion som en central förmåga som möjliggör lärande men även att de sällan funderar på vad som skulle kunna förbättra denna förmåga. De är därför även relativt främmande till ett meta-kognitivt angreppssätt på den neurovetenskapliga forskningen vilken enligt forskarna skulle kunna underlätta för elevernas styrning av sin koncentration genom att medvetandegöra dem.