| 1. |
- Andersson, Håkan, 1974-
(författare)
-
Childhood Self-Regulation, Academic Achievement, and Occupational Attainment
- 2012
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- The general aim of this thesis was to extend knowledge of the interplay between self-regulation (SR) skills during childhood in relation to academic achievement and later adult educational and occupational attainment. Previous research has shown that cool SR (i.e., cognitive) is more closely linked to academic achievement than hot SR (i.e., motivational/emotional). However, studies investigating both cool and hot SR in relation to academic achievement have been restricted to young children. Therefore, Study I assessed cool and hot SR in relation to academic achievement over a longer time period. The results showed that cool SR at age 3 was related to achievement already at age 6. Hot SR at age 3 did not predict achievement until later on in elementary school. Study II investigated the contribution of interference control and attention skills at age 6 to concurrent and later academic achievement at age 10. As the learning material becomes increasingly more complex throughout elementary school and teachers may give less support, interference control was expected to have a delayed effect on academic achievement relative to attention skills. Results showed that attention skills were related to academic achievement at age 6, whereas interference control only predicted academic achievement at age 10. Study III investigated task persistence in young adolescence in relation to academic achievement later in school and educational and occupational attainment in midlife. Results showed that task persistence contributed to change in grades between ages 13 and 16. Further, task persistence predicted later educational and occupational attainment (men only). Importantly, individual differences in intelligence, motivation, social background, and later educational attainment did not account for these effects. The findings point to a fundamental role of self-regulation in childhood for successful academic achievement and later attainment in adulthood.
|
|
| 2. |
- Bergman, Petra
(författare)
-
Genetic and epigenetic factors shaping the transcriptome in multiple sclerosis and its animal model
- 2014
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Multiple Sclerosis (MS) is a chronic inflammatory and demyelinating disease of the central nervous system. Susceptibility to develop MS is determined by both genetic and environmental factors. The epigenome resides in the interface of genetic and environmental factors thereby shaping the transcriptome. Furthermore, epigenetic mechanisms have been implicated in the etiology of MS. Epigenetics refers to changes in gene expression that are not a result of alterations in DNA sequence. Epigenetic mechanisms include histone modifications, DNA methylation and non-coding RNAs. MicroRNAs (miRNAs), small non-coding RNAs known to regulate gene expression, have been found dysregulated in most diseases, including MS. This thesis utilizes an animal model of MS, experimental autoimmune encephalomyelitis (EAE), to investigate epigenetic mechanisms and miRNAs as mediators and modulators of autoimmunity. Through the use of a knockout mouse model we demonstrated that histone demethylase Kdm3a is not a ‘master regulator’ of EAE. However, we demonstrated that a genetic variant in the rat Kdm3a affects nucleotide secondary structure and potentially protein translation. The role of epigenetic mechanisms was demonstrated by the identification of parent-of-origin dependent effects (such as genomic imprinting) in the inheritance of EAE. Using next generation sequencing we established a miRNA profile that associates with pathogenic immune activation in rat EAE, with potential miRNA-depended regulation of several important functions in the development of autoimmunity. Furthermore, by investigating the potential of circulating miRNAs as biomarkers of MS, we identified miR-150 as a putative novel biomarker for MS in the cerebrospinal fluid. Collectively, we show that modulation of the transcriptome by epigenetic mechanisms and miRNAs can explain more of the unknown underlying factors regulating susceptibility to autoimmune diseases and that dysregulated miRNAs can serve as markers of ongoing pathogenesis
|
|
| 3. |
|
|
| 4. |
- Bergman, Petra, et al.
(författare)
-
Next-generation sequencing identifies microRNAs that associate with pathogenic autoimmune neuroinflammation in rats.
- 2013
-
Ingår i: Journal of Immunology. - : The American Association of Immunologists. - 0022-1767 .- 1550-6606. ; 190:8, s. 4066-75
-
Tidskriftsartikel (refereegranskat)abstract
- MicroRNAs (miRNAs) are known to regulate most biological processes and have been found dysregulated in a variety of diseases, including multiple sclerosis (MS). In this study, we characterized miRNAs that associate with susceptibility to develop experimental autoimmune encephalomyelitis (EAE) in rats, a well-established animal model of MS. Using Illumina next-generation sequencing, we detected 544 miRNAs in the lymph nodes of EAE-susceptible Dark Agouti and EAE-resistant Piebald Virol Glaxo rats during immune activation. Forty-three miRNAs were found differentially expressed between the two strains, with 81% (35 out of 43) showing higher expression in the susceptible strain. Only 33% of tested miRNAs displayed differential expression in naive lymph nodes, suggesting that a majority of regulated miRNAs are EAE dependent. Further investigation of a selected six miRNAs indicates differences in cellular source and kinetics of expression. Several of the miRNAs, including miR-146a, miR-21, miR-181a, miR-223, and let-7, have previously been implicated in immune system regulation. Moreover, 77% (33 out of 43) of the miRNAs were associated with MS and other autoimmune diseases. Target genes likely regulated by the miRNAs were identified using computational predictions combined with whole-genome expression data. Differentially expressed miRNAs and their targets involve functions important for MS and EAE, such as immune cell migration through targeting genes like Cxcr3 and cellular maintenance and signaling by regulation of Prkcd and Stat1. In addition, we demonstrated that these three genes are direct targets of miR-181a. Our study highlights the impact of multiple miRNAs, displaying diverse kinetics and cellular sources, on development of pathogenic autoimmune inflammation.
|
|
| 5. |
- Duell, Eric J, et al.
(författare)
-
Menstrual and reproductive factors, exogenous hormone use, and gastric cancer risk in a cohort of women from the European Prospective Investigation Into Cancer and Nutrition
- 2010
-
Ingår i: American Journal of Epidemiology. - : Oxford University Press (OUP). - 0002-9262 .- 1476-6256. ; 172:12, s. 1384-1393
-
Tidskriftsartikel (refereegranskat)abstract
- The worldwide incidence of gastric adenocarcinoma (GC) is lower in women than in men. Furthermore, cancer patients treated with estrogens have been reported to have a lower subsequent risk of GC. The authors conducted a prospective analysis of menstrual and reproductive factors, exogenous hormone use, and GC in 335,216 women from the European Prospective Investigation Into Cancer and Nutrition, a cohort study of individuals aged 35-70 years from 10 European countries. After a mean follow-up of 8.7 years (through 2004), 181 women for whom complete exposure data were available developed GC. Adjusted hazard ratios and 95% confidence intervals were estimated using Cox proportional hazards models. All statistical tests were 2-sided. Women who had ovariectomy had a 79% increased risk of GC (based on 25 cases) compared with women who did not (hazard ratio = 1.79, 95% confidence interval: 1.15, 2.78). Total cumulative years of menstrual cycling was inversely associated with GC risk (fifth vs. first quintile: hazard ratio = 0.55, 95% confidence interval: 0.31, 0.98; P(trend) = 0.06). No other reproductive factors analyzed were associated with risk of GC. The results of this analysis provide some support for the hypothesis that endogenous ovarian sex hormones lower GC incidence in women.
|
|
| 6. |
- Gunnmo, Petra, et al.
(författare)
-
What do individuals with schizophrenia need to increase their well-being
- 2011
-
Ingår i: International Journal of Qualitative Studies on Health and Well-being. - : Informa UK Limited. - 1748-2623 .- 1748-2631. ; 6:1, s. 5412-
-
Tidskriftsartikel (refereegranskat)abstract
- The aim of this qualitative study was to deepen the knowledge of how individuals with schizophrenia themselves describe what they need in order to increase their well-being in everyday life. Seven patients were interviewed. An open explorative approach was applied and grounded theory was used for the analysis resulting in five categories illustrating how patients with schizophrenia handle their struggle for a normal life. The patients stressed first the importance of receiving information about the disease: for themselves, for society, and for their families. Taking part in social contacts such as attending meeting places and receiving home visits were identified as important as well as having meaningful employment. They also pointed out the importance of taking part in secure professional relationships. Mainly they expressed the need for continuity in the relationships and the wish to be heard and seen by the professionals. Finally, interviewees addressed the need for support for sustaining independent living through practical housekeeping and financial help. To conclude, the participants in the present study described their need for help as mainly linked to activities in their overall life situation rather than just their psychosis.
|
|
| 7. |
- Kotarsky, Heike, et al.
(författare)
-
Characterization of complex III deficiency and liver dysfunction in GRACILE syndrome caused by a BCS1L mutation.
- 2010
-
Ingår i: Mitochondrion. - : Elsevier BV. - 1567-7249. ; Jul 1, s. 497-509
-
Tidskriftsartikel (refereegranskat)abstract
- A homozygous mutation in the complex III chaperone BCS1L causes GRACILE syndrome (intrauterine growth restriction, aminoaciduria, cholestasis, hepatic iron overload, lactacidosis). In control and patient fibroblasts we localized BCS1L in inner mitochondrial membranes. In patient liver, kidney, and heart BCS1L and Rieske protein levels, as well as the amount and activity of complex III, were decreased. Major histopathology was found in kidney and liver with cirrhosis and iron deposition, but of iron-related proteins only ferritin levels were high. In placenta from a GRACILE fetus, the ferrooxidases ceruloplasmin and hephaestin were upregulated suggesting association between iron overload and placental dysfunction.
|
|
