| 1. |
- Wallsten, Daniel, et al.
(författare)
-
Treating co-morbid insomnia and social anxiety disorder with sequential CBT protocols : a single-case experimental study
- 2021
-
Ingår i: Behavioural and Cognitive Psychotherapy. - : Cambridge University Press. - 1352-4658 .- 1469-1833. ; 49:6, s. 641-657
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Although insomnia disorder and social anxiety disorder are among the most prevalent psychiatric disorders, no studies have yet evaluated the use of sequential evidence-based treatment protocols in the population with co-morbid social anxiety disorder and insomnia disorder.AIMS: This study aimed to investigate the effects of sequential treatments on co-morbid insomnia disorder and social anxiety disorder. As depression is a common co-morbid syndrome for both insomnia and social anxiety, a secondary aim was to examine depressive symptoms.METHOD: A single-case repeated crossover AB design was used. Ten participants between 18 and 59 years of age with co-morbid DSM-5 diagnoses of insomnia disorder and social anxiety disorder received sequential treatments with cognitive behavioural therapy (CBT). Seven participants completed the treatment course. The primary outcomes were symptoms of insomnia and social anxiety, and the secondary outcome was symptoms of depression.RESULTS: The effects of CBT on people with co-morbid social anxiety disorder and insomnia disorder were mixed. The majority of participants improved their sleep quality and lessened symptoms of social anxiety and depression. However, participants differed in their degree of improvement concerning all three disorders.CONCLUSIONS: Sequential CBT treatments are potentially effective at decreasing symptoms of social anxiety and insomnia for people with co-morbid social anxiety disorder and insomnia disorder. The variation in outcome across participants makes firm conclusions about the treatment efficacy difficult to draw.
|
|
| 2. |
|
|
| 3. |
|
|
| 4. |
|
|
| 5. |
|
|
| 6. |
- Elmabsout, Ali Ateia, et al.
(författare)
-
Cloning and Functional Studies of a Splice Variant of CYP26B1 Expressed in Vascular Cells
- 2012
-
Ingår i: Plos One. - San Francisco, USA : Public Library of Science (PLoS). - 1932-6203. ; 7:5
-
Tidskriftsartikel (refereegranskat)abstract
- Background: All-trans retinoic acid (atRA) plays an essential role in the regulation of gene expression, cell growth and differentiation and is also important for normal cardiovascular development but may in turn be involved in cardiovascular diseases, i.e. atherosclerosis and restenosis. The cellular atRA levels are under strict control involving several cytochromes P450 isoforms (CYPs). CYP26 may be the most important regulator of atRA catabolism in vascular cells. The present study describes the molecular cloning, characterization and function of atRA-induced expression of a spliced variant of the CYP26B1 gene. Methodology/Principal Findings: The coding region of the spliced CYP26B1 lacking exon 2 was amplified from cDNA synthesized from atRA-treated human aortic smooth muscle cells and sequenced. Both the spliced variant and full length CYP26B1 was found to be expressed in cultured human endothelial and smooth muscle cells, and in normal and atherosclerotic vessel. atRA induced both variants of CYP26B1 in cultured vascular cells. Furthermore, the levels of spliced mRNA transcript were 4.5 times higher in the atherosclerotic lesion compared to normal arteries and the expression in the lesions was increased 20-fold upon atRA treatment. The spliced CYP26B1 still has the capability to degrade atRA, but at an initial rate one-third that of the corresponding full length enzyme. Transfection of COS-1 and THP-1 cells with the CYP26B1 spliced variant indicated either an increase or a decrease in the catabolism of atRA, probably depending on the expression of other atRA catabolizing enzymes in the cells. Conclusions/Significance: Vascular cells express the spliced variant of CYP26B1 lacking exon 2 and it is also increased in atherosclerotic lesions. The spliced variant displays a slower and reduced degradation of atRA as compared to the full-length enzyme. Further studies are needed, however, to clarify the substrate specificity and role of the CYP26B1 splice variant in health and disease.
|
|
| 7. |
|
|
| 8. |
|
|
| 9. |
|
|
| 10. |
- Fagan, V., et al.
(författare)
-
COMPARE analysis of the toxicity of an iminoquinone derivative of the imidazo[5,4-f]benzimidazoles with NAD(P)H:quinone Oxidoreductase 1 (NQO1) activity and computational docking of quinones as NQO1 substrates
- 2012
-
Ingår i: Bioorganic & Medicinal Chemistry. - : Elsevier BV. - 0968-0896 .- 1464-3391. ; 20:10, s. 3223-3232
-
Tidskriftsartikel (refereegranskat)abstract
- Synthesis and cytotoxicity of imidazo[5,4-f]benzimidazolequinones and iminoquinone derivatives is described, enabling structure-activity relationships to be obtained. The most promising compound (an iminoquinone derivative) has undergone National Cancer Institute (NCI) 60 cell line (single and five dose) screening, and using the NCI COMPARE program, has shown correlation to NQO1 activity and to other NQO1 substrates. Common structural features suggest that the iminoquinone moiety is significant with regard to NQO1 specificity. Computational docking into the active site of NQO1 was performed, and the first comprehensive mitomycin C (MMC)-NQO1 docking study is presented. Small distances for hydride reduction and high binding affinities are characteristic of MMC and of iminoquinones showing correlations with NQO1 via COMPARE analysis. Docking also indicated that the presence of a substituent capable of hydrogen bonding to the His194 residue is important in influencing the orientation of the substrate in the NQO1 active site, leading to more efficient reduction. (C) 2012 Elsevier Ltd. All rights reserved.
|
|
