| 1. |
- Pourhamidi, Kaveh, et al.
(författare)
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Heat shock protein 27 concentrations are lower in patientswith type 1 diabetes mellitus than in healthy controls andcorrelates with large nerve fibre dysfunction
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- Objective Heat shock protein 27 (HSP27) may contribute to the survival of neurons. Our aims were to study whether HSP27 concentrations differ between individuals with and without type 1 diabetes, and evaluate the relationship between the progression of peripheral nerve dysfunction and HSP27 concentrations.Research Design and Methods Type 1 diabetes patients (n=27, 41% women; mean age 41±8 years) were recruited in 1992 with a follow-up in 2005; serum HSP27 concentrations were determined in baseline and follow-up samples and compared to non-diabetic controls (n=397, 34% women; mean age 43±14 years). The type 1 diabetes patients underwent nerve conduction studies and thermal and vibration perception threshold tests at baseline and at follow-up. Reference data was used to standardise results for age, height and sex by calculating the Z-scores. Delta changes in HSP27 (follow-up HSP27 – baseline HSP27) and small and large nerve fibre function were used for correlation analyses.Results Type 1 diabetes patients had lower HSP27 concentrations at baseline (mean HSP27547 pg/ml, 95% CI 421, 711) and at follow-up (mean HSP27 538 pg/ml, 95% CI 417,693) compared to healthy controls (mean HSP27 785 pg/ml, 95% CI 732, 842; p<0.05 for both comparisons). Deteriorating large nerve fibre function correlated with delta HSP27 concentrations in type 1 diabetes (r=0.50, p=0.01).Conclusions Patients with type 1 diabetes had lower HSP27 concentrations than non-diabetic controls and progression of large nerve fibre dysfunction correlated with decreasing HSP27 concentrations during the follow-up period. This could be indicative ofinsufficient neuroprotection in type 1 diabetes.
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| 2. |
- Bergemalm, Daniel, 1977-, et al.
(författare)
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Superoxide dismutase-1 and other proteins in inclusions from transgenic amyotrophic lateral sclerosis model mice
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- Mutant superoxide dismutase-1 (SOD1) causes amyotrophic lateral sclerosis (ALS) through a cytotoxic mechanism of unknown nature. A hallmark in ALS patients and transgenic mouse models carrying human SOD1 (hSOD1) mutations are hSOD1-immunoreactive inclusions in spinal cord ventral horns. The hSOD1 inclusions may block essential cellular functions or cause toxicity through sequestering of other proteins. Inclusions from 4 different transgenic mouse models were examined after density gradient ultracentrifugation. The inclusions are complex structures with heterogeneous densities and are disrupted by detergents. The aggregated hSOD1 was mainly composed of subunits that lacked the native stabilizing intrasubunit disulfide bond. A proportion of subunits formed hSOD1 oligomers or was bound to other proteins through disulfide bonds. Dense inclusions could be isolated and the protein composition was analyzed using proteomic techniques. Mutant hSOD1 accounted for half of the protein. Ten other proteins were identified. Two were cytoplasmic chaperones, 4 were cytoskeletal proteins, and 4 were proteins that normally reside in the endoplasmic reticulum (ER). The presence of ER proteins in inclusions containing the primarily cytosolic hSOD1 further supports the notion that ER stress is involved in ALS.
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| 3. |
- Gustafsson, Mika, 1977-, et al.
(författare)
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Data for: Proteomics reveal biomarkers for diagnosis, disease activity and long-term disability outcomes in multiple sclerosis
- 2023
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Annan publikationabstract
- Protein levels were measured in cerebrospinal fluid samples (CSF; n = 186) and plasma samples (n = 165) from persons with multiple sclerosis and healthy controls. CSF samples and plasma samples were taken from 92 persons with CIS or RRMS at Linköping University Hospital, Sweden and 51 persons with CIS or RRMS at the Karolinska University Hospital, Sweden. Everyone fulfilled the revised McDonald criteria from 2010 and 2017 for CIS or Multiple sclerosis (MS). Age-matched healthy controls (HC) were recruited from healthy blood donors (23 at the Linköping University hospital and 20 at the Karolinska University Hospital). The concentration of 1463 proteins were measured using the Olink Explore platform which uses Proximity Extension Assay (PEA) technology. The proteins were preselected from four Olink panels: Explore 384 Cardiometabolic, Explore 384 Inflammation, Explore 384 Neurology, and Explore 384 Oncology. The protein concentrations are given as Olink’s relative protein quantification unit on log2 scale: Normalized Protein Expression (NPX). The NPX values were intensity normalized by Olink.
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| 4. |
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| 5. |
- Malmgren, Helge, 1945
(författare)
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Classical Rorschach
- 2004
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Ingår i: Internet.
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- These web pages are devoted to the presentation and promotion of the Rorschach method, concentrating on the way it has been practiced within the classical European tradition - from Hermann Rorschach himself in 1921, via Ewald Bohm in the 1950's, 1960's and 1970's, and to the contemporary workers in the Rorschach-Bohm tradition. You can here find basic information about Hermann Rorschach, about the different Rorschach traditions and the essential differences between them, and about the current scientific debate about the Rorschach test. There are also some links to other Web pages devoted to the Rorschach method. The information on these pages has been carefully selected so that it can be made publicly available without interferring with the clinical and scientific use of the Rorschach test. Hence no specific information about the test procedure, about response categories and so on has been included, and of course no pictures of the Rorschach cards are shown.
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| 6. |
- Nordanskog, Pia, et al.
(författare)
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Relative decrease of frontal blood flow after electroconvulsive therapy in depression distinguishes remission: a perfusion MRI study
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- Background: Understanding electroconvulsive therapy (ECT) is of importance not only for optimizing treatment, but could also provide important information about key features of the healing process in depression. Enhanced inhibition (the anticonvulsant hypothesis) is one of several suggested mechanisms of action of ECT. Earlier studies on cerebral blood flow during ECT have given diverging results. Our aim was to study changes in cerebral blood flow in depression treated with ECT and their relation to treatment outcome.Methods: We obtained MRI scans in 14 depressed subjects referred for ECT. Cerebral blood flow (CBF) was measured using dynamic susceptibility contrast magnetic resonance imaging (DSC-MRI) within 1 week before and 2 weeks after a course of ECT. The relative CBF was calculated from mean values in predefined regions of interest in relation to the mean value in the whole brain.Results: A significant relative CBF increase in the occipital region (p < 0.05) and a significant relative decrease in the right lateral temporal lobe (p < 0.05) were found in the entire study group. A significant decrease in the right frontal lobe, with a significant anteriorposterior and right-left gradient shift in relative CBF, was a distinguishing feature in patients with ECT-induced remission (n = 8).Limitations: This observational study is limited by the risk of random bias and its low number of participants.Conclusions: Our results suggest that a decreased relative blood flow in frontal regions may be a hallmark of treatment efficacy in depression treated with ECT.
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| 7. |
- de Flon, Pierre, 1966-, et al.
(författare)
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Comparison of plasma and CSF Neurofilament light as outcome in a multiple sclerosis trial
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- Objective: The main objective of this study was to evaluate the axonal component neurofilament light protein (NFL) in plasma and cerebrospinal fluid (CSF) as an outcome measure in a clinical trial on disease-modifying treatments in multiple sclerosis.Method: Seventy-five patients with clinically stable relapsing-remitting multiple sclerosis (RRMS) participating in the clinical trial “Switch-To RItuXimab in MS” (STRIX-MS) were switched to rituximab from first-line injectable therapy and then followed for two years. Thirty patients from the extension trial (STRIX-MS extension), accepting repeated lumbar punctures, were followed for an additional three years. Plasma and CSF samples were collected yearly during the follow-up. NFL concentration in plasma was measured by an in-house NF-light assay on the Simoa platform with a Homebrew kit. NFL concentration in CSF was measured by sandwich ELISA.Results: The mean levels of NFL, in both CSF and plasma, were low. The reduction of CSF-NFL with 25% during the first year of follow-up (from a mean of 471 (SD 393) to 354 (SD 174) pg/mL; p=0.006) was statistically significant. The corresponding reduction in plasma-NFL was 18% (from 9.73 (SD 7.04) to 7.94 (SD 3.10) pg/mL; p=0.055) and did not reach the level of statistical significance.Conclusion: This study indicates that NFL in plasma is less sensitive as an endpoint in group comparisons than NFL in CSF. Given that plasma NFL is far easier to access, it is a promising and awaited method but further studies are needed to optimise the use in clinical trials.
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| 8. |
- Emami Khoonsari, Payam, et al.
(författare)
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Chitinase-3-like protein 1 (CH3L1) and Neurosecretory protein VGF (VGF) as two novel CSF biomarker candidates for improved diagnostics in Alzheimer’s disease
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- Alzheimer’s disease (AD) is a chronic neurodegenerative disorder characterized by amyloid-β (Aβ) plaque deposition and accumulation of intracellular neurofibrillary tangles. This pathology is mirrored in the cerebrospinal fluid (CSF), where decreased Aβ42 together with increased total (t-tau) and phospho-tau (p-tau) today is used as a diagnostic marker. Although these biomarkers have a fairly good sensitivity and specificity, additional biomarkers are needed to further improve the accuracy for early disease detection and to monitor disease development. In this study, we used mass spectrometry-based shotgun proteomics to investigate the CSF proteome of patients with AD and mild cognitive impairment (MCI) as well as of non-demented controls. By combining the diagnostic markers (Aβ42, total t-tau, and p-tau) with a selection of proteomics biomarkers, the accuracy of predicting MCI to AD conversion increased from 83% to 92% with a specificity of 1.0 and sensitivity of 0.86. Among these markers, the levels of protein chitinase-3-like protein 1 (CH3L1) were significantly higher in AD and MCI converters compared to controls. In addition to Aβ42, t-tau, and p-tau the protein CH3L1 contributed mostly to the prediction accuracy. We also found statistically significant lower CSF levels of the neurosecretory protein VGF (VGF) in AD compared to controls. Taken together, our findings suggest that incorporating new CSF biomarkers can further enhance early diagnosis of AD.
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