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- Jensen, Karin B, et al.
(författare)
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Cognitive Behavioral Therapy increases pain-evoked activation of the prefrontal cortex in patients with fibromyalgia.
- 2012
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Ingår i: Pain. - : Ovid Technologies (Wolters Kluwer Health). - 0304-3959 .- 1872-6623. ; 153:7, s. 1495-1503
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Tidskriftsartikel (refereegranskat)abstract
- Interventions based on Cognitive Behavioral Therapy (CBT) are widely used to treat chronic pain, but the brain mechanisms responsible for these treatment effects are poorly understood. The aim of this study was to validate the relevance of the cortical control theory in response to an exposure-based form of CBT, Acceptance and Commitment Therapy, in patients with chronic pain. Forty-three female patients diagnosed with fibromyalgia syndrome were enrolled in a randomized, 12-week, waiting-list controlled clinical trial (CBT n=25; controls n=18). CBT was administered in groups of six patients during 12 weekly sessions. Functional magnetic resonance imaging (fMRI) during pressure-evoked pain was assessed before and after treatment or the 12-week period. Self-report questionnaires of depression and anxiety were administered pre- and posttreatment as well as 3 months following end of treatment. Patients treated with CBT reported larger improvement of fibromyalgia on the Patient Global Impression of Change measure, and improved depression and anxiety symptoms, compared to the waiting-list controls. However, there were no effects on clinical pain or pain sensitivity measures. An analysis of fMRI scans revealed that CBT led to increased activations in the ventrolateral prefrontal/lateral orbitofrontal cortex; regions associated with executive cognitive control. We suggest that CBT changes the brain's processing of pain through an altered cerebral loop between pain signals, emotions, and cognitions; leading to increased access to executive regions for reappraisal of pain. Our data thereby support our hypothesis about the activation of a cortical control mechanism in response to CBT treatment in chronic pain.
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| 2. |
- Nguyen, Sang N., et al.
(författare)
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Methodology for predicting the threat of runway debris impact to large transport aircraft
- 2012
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Konferensbidrag (refereegranskat)abstract
- Large transport aircraft are particularly susceptible to impact damage from runway debris thrown up by the landing gear. A methodology was developed to predict the trajectories of stones lofted by the nose wheel and subjected to aerodynamics forces due to the wake behind the nose landing gear and beneath the aircraft. In conjunction with finite element modeling of the stone/ground/tire contact mechanics, a Matlab model was used to perform a stochastic prediction of the trajectories of runway stones to generate impact threat maps which showed the relative likelihood of stones impinging upon various areas on the underside of a C-130 Hercules. The impact envelopes for the C-130 extended 2.4 to 17.5 meters behind the nose wheel and two meters either side of the center of the aircraft. The impact threat maps were especially sensitive to the values of the coefficients of lift and drag acting on the stone during its flight.
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| 3. |
- Olsson, Mike, et al.
(författare)
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Machinability of Ductile Single-Phase Materials Used in Accelerator Components - A Study with Focus on Surface Integrity
- 2014
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Ingår i: Proceedings of the 6th Swedish Production Symposium.
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Konferensbidrag (refereegranskat)abstract
- The focus of this article has been to analyse the machinability, with focus on surface integrity, of oxygen-free copper (OFC) and niobium during turning operations. The results from machining OFC proved that all of the tools that was tested can be used to achieve a surface roughness below Ra = 0.8 µm with the correct cutting data. From the results when machining niobium it showed that only the cemented carbide tool with a nose radius of 1.2 mm was able to achieve a surface roughness of Ra = 0.8 µm or greater. The cutting resistance based on the measured cutting forces was high for both of the materials.
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| 4. |
- Sawcer, Stephen, et al.
(författare)
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Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis
- 2011
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Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 476:7359, s. 214-219
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Tidskriftsartikel (refereegranskat)abstract
- Multiple sclerosis is a common disease of the central nervous system in which the interplay between inflammatory and neurodegenerative processes typically results in intermittent neurological disturbance followed by progressive accumulation of disability. Epidemiological studies have shown that genetic factors are primarily responsible for the substantially increased frequency of the disease seen in the relatives of affected individuals, and systematic attempts to identify linkage in multiplex families have confirmed that variation within the major histocompatibility complex (MHC) exerts the greatest individual effect on risk. Modestly powered genome-wide association studies (GWAS) have enabled more than 20 additional risk loci to be identified and have shown that multiple variants exerting modest individual effects have a key role in disease susceptibility. Most of the genetic architecture underlying susceptibility to the disease remains to be defined and is anticipated to require the analysis of sample sizes that are beyond the numbers currently available to individual research groups. In a collaborative GWAS involving 9,772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the HLA-DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the class I region. Immunologically relevant genes are significantly overrepresented among those mapping close to the identified loci and particularly implicate T-helper-cell differentiation in the pathogenesis of multiple sclerosis.
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| 5. |
- Warnke, Clemens, et al.
(författare)
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Cerebrospinal Fluid JC Virus Antibody Index for Diagnosis of Natalizumab-Associated Progressive Multifocal Leukoencephalopathy
- 2014
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Ingår i: Annals of Neurology. - : Wiley. - 0364-5134 .- 1531-8249. ; 76:6, s. 792-801
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Progressive multifocal leukoencephalopathy (PML), caused by JC virus (JCV), can occur in patients receiving natalizumab for multiple sclerosis (MS). JCV detection by quantitative polymerase chain reaction (qPCR) in cerebrospinal fluid (CSF), or brain biopsy, is required for probable or definite diagnosis of PML. However, in some patients only low levels of JCV DNA (<100 copies/ml) are present in CSF, making the diagnosis challenging. Our objective was to assess the complementary value of a CSF JCV antibody index (AI(JCV)) in the diagnosis of natalizumab-associated PML.Methods: AI(JCV) was assessed in 37 cases of natalizumab-associated PML and 89 MS-patients treated with natalizumab without PML. Sera and CSF were tested in a capture enzyme-linked immunosorbent assay, using JCV-VP1 fused to glutathione S-transferase as antigen. Albumin levels and total immunoglobulin G concentration were determined by immunonephelometry, and the AI(JCV) was calculated as published.Results:Twenty-six of 37 (70%) patients with natalizumab-associated PML exhibited an AI(JCV) > 1.5, whereas this was seen in none of the controls (p < 0.0001). At time of the first positive qPCR for JCV DNA, 11 of 20 (55%) patients with natalizumab-associated PML had an AI(JCV) > 1.5. JCV DNA levels of <100 copies/ml were seen in 14 (70%) of these 20 patients, of whom 8 (57%) demonstrated an AI(JCV) > 1.5.Interpretation: Determination of the AI(JCV) could be an added tool in the diagnostic workup for PML and should be included in the case definition of natalizumab-associated PML. Ann Neurol 2014;76:792-801
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