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| 2. |
- Ekman, Anna-Karin, et al.
(author)
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Systemically elevated Th1-, Th2- and Th17-associated chemokines in psoriasis vulgaris before and after ultraviolet B treatment
- 2013
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In: Acta Dermato-Venereologica. - : Society for Publication of Acta Dermato-Venereologica. - 0001-5555 .- 1651-2057. ; 93:5, s. 527-531
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Journal article (peer-reviewed)abstract
- Chemokines may contribute to the systemic inflammation that is linked to the increased risk of co-morbidities in patients with psoriasis. The aim of this study was to investigate circulating chemokines in patients with psoriasis and their relationship to disease severity. Analysis of plasma levels of chemokines in patients with psoriasis before narrowband ultraviolet B (UVB) therapy revealed increased expression of Th1-associated CXCL9 and -10, Th2-associated CCL17 and CCL22, and Th17-associated CCL20. CCL20 correlated with disease severity. UVB therapy reduced skin symptoms, but did not affect the chemokine levels in plasma. Anti-CD3 and anti-CD28-mediated activation of peripheral blood mononuclear cells (PBMCs) caused a higher secretion of Th2 cytokine interleukin (IL)-13 by PBMCs from patients with psoriasis than from healthy controls. The sustained high expression of inflammatory chemokines is a potential link to systemic inflammation in psoriasis. UVB therapy may be a more effective treatment of local rather than systemic inflammation.
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| 3. |
- Anckarsäter, Henrik, 1966, et al.
(author)
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Child neurodevelopmental and behavioural problems are intercorrelated and dimensionally distributed in the general population
- 2008
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In: The Open Psychiatry Journal. - : Bentham Science Publishers Ltd.. - 1874-3544. ; 2, s. 5-11
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Journal article (peer-reviewed)abstract
- The Autism – Tics, AD/HD, and other Comorbidities inventory (A-TAC) is a comprehensive interview for evaluating problems related to autism spectrum disorders (ASD), tic disorders, attention-deficit/hyperactivity disorder (AD/HD), and common comorbid conditions in children and adolescents. A-TAC telephone interviews were administered to parents of 2,957 children aged nine- or twelve-years, representing one in each twin pair included in the population- based Child and Adolescent Twin Study in Sweden (CATSS). A total of 16.4% were screen-positive for one or several of the targeted disorder, 1.3% for ASD and 5.6% for AD/HD. All types of problems were more common among boys, with the exception of those related to “eating habits”. They were all dimensionally/continuously distributed, highly inter-correlated, and overlapped across types. They aggregated in three ba- sic factors corresponding to externalizing/disruptiveness, socio-communicative problems, and compulsiveness. Population-based data on problems in children thus challenge current categorical diagnostic definitions, calling for dimen- sional and complementary models of problem descriptions.
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| 4. |
- Anckarsäter, Henrik, 1966, et al.
(author)
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The Child and Adolescent Twin Study in Sweden (CATSS).
- 2011
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In: Twin Research and Human Genetics. - : Cambridge University Press (CUP). - 1832-4274 .- 1839-2628. ; 14:6, s. 495-508
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Journal article (peer-reviewed)abstract
- The Child and Adolescent Twin Study in Sweden (CATSS) is an ongoing longitudinal twin study targeting all twins born in Sweden since July 1, 1992. Since 2004, parents of twins are interviewed regarding the children's somatic and mental health and social environment in connection with their 9th or 12th birthdays (CATSS-9/12). By January 2010, 8,610 parental interviews concerning 17,220 twins had been completed, with an overall response rate of 80%. At age 15 (CATSS-15) and 18 (CATSS-18), twins and parents complete questionnaires that, in addition to assessments of somatic and mental health, include measures of personality development and psychosocial adaptation. Twin pairs in CATSS-9/12 with one or both twins screening positive for autism spectrum disorders, attention deficit/hyperactivity disorder, tic disorders, developmental coordination disorder, learning disorders, oppositional defiant disorder, conduct disorder, obsessive-compulsive disorder, and/or eating problems have been followed with in-depth questionnaires on family, social environment and personality, and subsequently by clinical assessments at age 15 together with randomly selected population controls, including 195 clinically assessed twin pairs from the first 2 year cohorts (CATSS-15/DOGSS). This article describes the cohorts and study groups, data collection, and measures used. Prevalences, distributions, heritability estimates, ages at onset, and sex differences of mental health problems in the CATSS-9/12, that were analyzed and found to be overall comparable to those of other clinical and epidemiological studies. The CATSS study has the potential of answering important questions on the etiology of childhood mental health problems and their role in the development of later adjustment problems.
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| 6. |
- Carlström, Mattias, et al.
(author)
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Cross-talk Between Nitrate-Nitrite-NO and NO Synthase Pathways in Control of Vascular NO Homeostasis
- 2015
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In: Antioxidants and Redox Signaling. - : Mary Ann Liebert Inc. - 1523-0864 .- 1557-7716. ; 23:4, s. 295-306
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Journal article (peer-reviewed)abstract
- Aims: Inorganic nitrate and nitrite from endogenous and dietary sources have emerged as alternative substrates for nitric oxide (NO) formation in addition to the classic L-arginine NO synthase (NOS)-dependent pathway. Here, we investigated a potential cross-talk between these two pathways in the regulation of vascular function. Results: Long-term dietary supplementation with sodium nitrate (0.1 and 1mmol kg(-1) day(-1)) in rats caused a reversible dose-dependent reduction in phosphorylated endothelial NOS (eNOS) (Ser1177) in aorta and a concomitant increase in phosphorylation at Thr495. Moreover, eNOS-dependent vascular responses were attenuated in vessels harvested from nitrate-treated mice or when nitrite was acutely added to control vessels. The citrulline-to-arginine ratio in plasma, as a measure of eNOS activity, was reduced in nitrate-treated rodents. Telemetry measurements revealed that a low dietary nitrate dose reduced blood pressure, whereas a higher dose was associated with a paradoxical elevation. Finally, plasma cyclic guanosine monophosphate increased in mice that were treated with a low dietary nitrate dose and decreased with a higher dose. Innovation and Conclusions: These results demonstrate the existence of a cross-talk between the nitrate-nitrite-NO pathway and the NOS-dependent pathway in control of vascular NO homeostasis. Antioxid. Redox Signal. 23, 295-306.
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| 7. |
- Carlström, Maria, 1975
(author)
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Effects of Biomechanical Stress on Gene Regulation in Vascular Cells
- 2007
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Doctoral thesis (other academic/artistic)abstract
- The vascular vessel wall is constantly exposed to biomechanical forces, such as shear and tensile stress. Biomechanical forces are important for several physiological and pathological processes and have been shown to regulate a number of fundamental vascular functions, such as vascular tone and remodeling processes. The aim of the present thesis was to study the effects of biomechanical forces on the vessel wall. Intact human conduit vessels were exposed to normal or high intraluminal pressure, or low or high shear stress in combination with a physiological level of the other factor in a unique vascular ex vivo perfusion model, developed in our laboratory. Global gene expression profiling was performed with microarray technology of endothelial cells from stimulated vessels. Biomechanical forces were found to regulate a large number of genes. The fraction of genes that responded to both pressure and shear stimulation was surprisingly low, which indicates that the two different stimuli induce distinct gene expression response patterns. Further, these results suggest that the endothelium has the capacity to discriminate between shear stress and pressure stimulation. Detection and quantification of changes in gene expression require valid and reliable endogenous references genes. Therefore, the appropriateness of ten reference genes for studies of biomechanically stimulated endothelium was evaluated by microarray technology and real-time RT-PCR. Shear stress plays an essential role in regulation of vascular tone and remodeling, and P2 receptors have been suggested to be mediators of some of these effects. We therefore studied the effects of shear stress on P2 receptor expression in intact human vessels. In the endothelium, no significant regulation of P2 receptor mRNA levels was observed. However, in smooth muscle cells, high shear stress decreased mRNA expression of the contractile P2X1 receptor and increased the mitogenic P2Y2 and P2Y6 receptors. These findings were consistent at the protein level with Western blot analysis and morphologically with immunohistochemistry. This suggests that the shear force can be transmitted to the underlying smooth muscle cells. The interplay of shear stress and inflammatory stress on urokinase-type plasminogen activator (u-PA) and plasminogen activator inhibitor-1 (PAI-1) expression was studied in an in vitro shear stress system. Endothelial cells were exposed to either shear stress, the proinflammatory cytokine tumor necrosis factor-? (TNF-a), or a combination of both. High shear stress markedly reduced u-PA expression whereas TNF-a induced u-PA expression. Combining shear stress and inflammatory stimulation reduced the TNF-a mediated u-PA induction, which suggests that shear stress exerts a strong protective effect. The TNF-a induced expression was proposed to be partly mediated by activation of c-jun N-terminal kinase (JNK). The PAI-1 expression was induced both by shear stress and TNF-a, and the effect was potentiated when the two stimuli were combined. In conclusion, these findings illustrate that biomechanical forces regulate a large number of genes in the endothelium and that shear stress and pressure induce distinct expression patterns. Shear stress also has the capacity to influence gene expression in smooth muscle cells in intact vessels and protect against inflammatory stress, which illustrates its potency as a regulator of endothelial cell function.
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| 9. |
- Carlström, Maria, et al.
(author)
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Genetic support for the role of the NLRP3 inflammasome in psoriasis susceptibility
- 2012
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In: Experimental dermatology. - : John Wiley and Sons. - 0906-6705 .- 1600-0625. ; 21:12, s. 932-937
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Journal article (peer-reviewed)abstract
- NACHT leucine-rich repeat- and PYD-containing (NLRP)3 protein controls the inflammasome by regulating caspase-1 activity and interleukin (IL)-1 beta processing. The contribution of IL-1 beta in the pathogenesis of psoriasis is well recognized. Polymorphisms in NLRP3 and caspase recruitment domaincontaining protein (CARD)8, a negative regulator of caspase-1 activity, have been associated with susceptibility to common inflammatory diseases, such as Crohns disease and rheumatoid arthritis. To investigate the role for genetic variants in the NLRP3 inflammasome in psoriasis susceptibility. In a patient sample comprising 1988 individuals from 491 families and 1002 healthy controls, genotypes for four selected single-nucleotide polymorphisms (SNPs) in NLRP3 (three SNPs) and CARD8 (one SNP) were determined by TaqMan (R) Allelic Discrimination. Using the transmission disequilibrium test (TDT), a significant increase in the transmission of the NLRP3 rs10733113G genotype to a subgroup of patients with more widespread psoriasis was demonstrated (P = 0.015). Using logistic regression analysis in 741 patients with psoriasis and 1002 controls, the CARD8 rs2043211 genotype was significantly different in cases and controls in overall terms [OR 1.3 (1.11.5), P = 0.004] and for both genders. Our data support the hypothesis that the inflammasome plays a role in psoriasis susceptibility.
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