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Sökning: (AMNE:(Clinical Medicine)) > (2010-2019)

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2.
  • Hedegärd, Emelie, et al. (författare)
  • Complications to invasive epilepsy surgery workup with subdural and depth electrodes: a prospective population-based observational study
  • 2014
  • Ingår i: Journal of Neurology Neurosurgery and Psychiatry. - : BMJ. - 0022-3050 .- 1468-330X. ; 85:7, s. 716-720
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective In some patients who undergo presurgical workup for drug-resistant epilepsy invasive seizure monitoring is needed to define the seizure onset zone and delineate eloquent cortex. Such procedures carry risks for complications causing permanent morbidity and even mortality. In this study, prospective data on complications in a national population-based sample were analysed. Design Complication data from the prospective Swedish National Epilepsy Surgery Register were analysed for 271 patients in whom therapeutic surgery was preceded by invasive monitoring 1996-2010. Results Complications occurred in 13/271 patients (4.8%). Subdural grids carried the highest risk of complications (7.4%). There was no surgical mortality or permanent morbidity. Subdural haematomas were most common (n=7) followed by epidural haematomas (n= 3). Valproate treatment and having a haematoma was associated with an OR of 1.53 (CI 0.38 to 6.12) compared to having a haematoma without valproate treatment. Having a complication during invasive monitoring was associated with a significant OR of 6.27 (CI 1.32 to 29.9) of also having a complication at therapeutic surgery compared to the risk of having a complication only at surgery. Conclusions In this prospective population-based epilepsy surgery series, the most common complications were haematomas, and subdural grids carried the highest risk. Close supervision and rapid interventions led to avoidance of permanent morbidity. The clinical implications of the slightly increased risk of haematomas with valproate treatment needs further investigation as does the finding of an increased risk for complications at epilepsy surgery for patients who had a complication during invasive monitoring.
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3.
  • Palmqvist, Sebastian, et al. (författare)
  • Detailed comparison of amyloid PET and CSF biomarkers for identifying early Alzheimer disease
  • 2015
  • Ingår i: Neurology. - : Lippincott Williams & Wilkins. - 1526-632X .- 0028-3878. ; 85:14, s. 1240-1249
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective:To compare the diagnostic accuracy of CSF biomarkers and amyloid PET for diagnosing early-stage Alzheimer disease (AD).Methods:From the prospective, longitudinal BioFINDER study, we included 122 healthy elderly and 34 patients with mild cognitive impairment who developed AD dementia within 3 years (MCI-AD). -Amyloid (A) deposition in 9 brain regions was examined with [F-18]-flutemetamol PET. CSF was analyzed with INNOTEST and EUROIMMUN ELISAs. The results were replicated in 146 controls and 64 patients with MCI-AD from the Alzheimer's Disease Neuroimaging Initiative study.Results:The best CSF measures for identifying MCI-AD were A42/total tau (t-tau) and A42/hyperphosphorylated tau (p-tau) (area under the curve [AUC] 0.93-0.94). The best PET measures performed similarly (AUC 0.92-0.93; anterior cingulate, posterior cingulate/precuneus, and global neocortical uptake). CSF A42/t-tau and A42/p-tau performed better than CSF A42 and A42/40 (AUC difference 0.03-0.12, p < 0.05). Using nonoptimized cutoffs, CSF A42/t-tau had the highest accuracy of all CSF/PET biomarkers (sensitivity 97%, specificity 83%). The combination of CSF and PET was not better than using either biomarker separately.Conclusions:Amyloid PET and CSF biomarkers can identify early AD with high accuracy. There were no differences between the best CSF and PET measures and no improvement when combining them. Regional PET measures were not better than assessing the global A deposition. The results were replicated in an independent cohort using another CSF assay and PET tracer. The choice between CSF and amyloid PET biomarkers for identifying early AD can be based on availability, costs, and doctor/patient preferences since both have equally high diagnostic accuracy.Classification of evidence:This study provides Class III evidence that amyloid PET and CSF biomarkers identify early-stage AD equally accurately.
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4.
  • Lewerin, Catharina, 1961, et al. (författare)
  • Low holotranscobalamin and cobalamins predict incident fractures in elderly men: the MrOS Sweden.
  • 2014
  • Ingår i: Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA. - : Springer Science and Business Media LLC. - 1433-2965 .- 0937-941X. ; 25:1, s. 131-140
  • Tidskriftsartikel (refereegranskat)abstract
    • In a population-based study on cobalamin status and incident fractures in elderly men (n=790) with an average follow-up of 5.9years, we found that low levels of metabolically active and total cobalamins predict incident fractures, independently of body mass index (BMI), bone mineral density (BMD), plasma total homocysteine (tHcy), and cystatin C.
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5.
  • Pourhamidi, Kaveh, 1985-, et al. (författare)
  • Association between symptoms of neuropathy, nerve conduction and levels of heat shock protein 27 in type 2 diabetes
  • 2010
  • Konferensbidrag (refereegranskat)abstract
    • Background and aims: Increased levels of serum HSP27 (sHSP27) are associated with distal symmetric polyneuropathy (DSPN) in type 1 diabetic patients. However, the association between nerve function and sHSP27 has not been studied in subjects with type 2 diabetes (T2D) and impaired glucose tolerance (IGT). Thus, our objectives were to investigate the association between nerve conduction in the legs, symptoms of distal polyneuropathy and sHSP27 levels. Methods: Subjects were consecutively recruited from the population-based Västerbotten Intervention Program; controls (n=39, m/f=19/20, mean age=61± 0.6 years), IGT (n=29, m/f=15/14, mean age=61± 0.8 years), T2D (n=51, m/f=30/21, mean age=61± 1.3 years). Nerve conduction studies were performed. Z-scores for motor conduction velocity (CV) of the peroneal nerve, and the sensory CV and amplitude of the sural nerve were measured and compiled into a composite Z-score of the right leg (Z-score leg). Neurological Disability Score (NDS), including examination of sensory perception, reflexes and muscle strength, were used to evaluate symptoms of neuropathy in the leg. NDS and Z-score leg were categorized into tertiles, respectively. sHSP27 levels were measured and divided into low and high levels. Results: Subjects in the highest NDS tertile had lower sHSP27 levels (328 ± 287 pg/mL) compared to subjects in the lowest NDS tertile (558 ± 404 pg/mL, p=0.04). Subjects in the lowest tertile of Z-score leg were in the lowest sHSP27 group (63%) compared to the subjects in the highest group (38%, p=0.034). The highest tertile of Z-score leg was associated with high levels of sHSP27 (OR 3.8, 95% CI 1.2; 11.5, p=0.02); adjusted for age and sex. However, this association was attenuated when adjusted for T2D status (OR 3.1, 95% CI 0.9; 9.9, p=0.06). Conclusion: In summary, increased sHSP27 levels were associated with an increasing Z-score of the leg; thus, a better nerve conduction, and fewer symptoms using the whole study population. The attenuation of the association when including diabetic status indicates an altered HSP27 production in T2D patients compared to controls and subjects with IGT.
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6.
  • Abtahi, Jahan, et al. (författare)
  • Bisphosphonate coating might improve fixation of dental implants in the maxilla: A pilot study
  • 2010
  • Ingår i: International Journal of Oral and Maxillofacial Surgery. - : Elsevier Science B.V., Amsterdam. - 0901-5027 .- 1399-0020. ; 39:7, s. 673-677
  • Tidskriftsartikel (refereegranskat)abstract
    • This pilot study evaluates the clinical stability of bisphosphonate-coated dental implants placed using a two-stage surgical procedure in five patients. Each patient received seven regular Brånemark implants, one of which was coated with bisphosphonate in a fibrinogen matrix. The coated implant was inserted where the bone was expected to have the least favourable quality. The level of the marginal bone around each implant was measured by intraoral periapical radiographs and implant stability was recorded using resonance frequency measurements. Frequency values (ISQ) were obtained peroperatively before flap closure and after 6 months at abutment connection. At abutment connection the bisphosphonate-coated implants were removed en bloc in two patients for histological examination. An animal experiment had previously confirmed that gamma-sterilization did not reduce bioactivity of the bisphosphonate coating. In each patient, the bisphosphonate-coated implant showed the largest improvement in ISQ level of all implants. Their values at the start tended to be lower, and the absolute value at 6 months did not differ. No complications occurred with the coated implants. Histology showed no abnormalities. Improvement in ISQ values was an expected effect of the bisphosphonate coating, but could be due to the choice of insertion site. This finding warrants a randomized, blinded study.
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7.
  • Schöll, Michael, 1980, et al. (författare)
  • Biomarkers for tau pathology.
  • 2019
  • Ingår i: Molecular and cellular neurosciences. - : Elsevier BV. - 1095-9327 .- 1044-7431. ; 97, s. 18-33
  • Forskningsöversikt (refereegranskat)abstract
    • The aggregation of fibrils of hyperphosphorylated and C-terminally truncated microtubule-associated tau protein characterizes 80% of all dementia disorders, the most common neurodegenerative disorders. These so-called tauopathies are hitherto not curable and their diagnosis, especially at early disease stages, has traditionally proven difficult. A keystone in the diagnosis of tauopathies was the development of methods to assess levels of tau protein in vivo in cerebrospinal fluid, which has significantly improved our knowledge about these conditions. Tau proteins have also been measured in blood, but the importance of tau-related changes in blood is still unclear. The recent addition of positron emission tomography ligands to visualize, map and quantify tau pathology has further contributed with information about the temporal and spatial characteristics of tau accumulation in the living brain. Together, the measurement of tau with fluid biomarkers and positron emission tomography constitutes the basis for a highly active field of research. This review describes the current state of biomarkers for tau biomarkers derived from neuroimaging and from the analysis of bodily fluids and their roles in the detection, diagnosis and prognosis of tau-associated neurodegenerative disorders, as well as their associations with neuropathological findings, and aims to provide a perspective on how these biomarkers might be employed prospectively in research and clinical settings.
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8.
  • Björkman, Kristoffer, et al. (författare)
  • Genotype-phenotype correlations in patients with complex I deficiency due to mutations in NDUFS1 and NDUFV1
  • 2014
  • Ingår i: Euromit 2014, 15-19 juni, Tampere, Finland.
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
    • Objectives: To study genotype-phenotype correlations in genes encoding complex I electron input module subunits. Materials and methods: We studied five patients with isolated complex I deficiency, three with NDUFS1 mutations and two with NDUFV1 mutations. A literature review of all reported cases of mutations in the affected genes was performed. Results: The literature review revealed pathological mutations in NDUFS1 for 18 patients in 17 families and correspondingly in NDUFV1 for 26 patients in 19 families. Unpublished clinical data for our five patients were added. Our study showed quite variable clinical courses; death before two years of age was seen in 41% of patients while 18% were alive at seven years. There was a significant difference between the NDUFS1 and NDUFV1 groups for clinical onset and life-span. Mutations in NDUFS1 were linked to a worse clinical course with earlier onset and earlier death. Conclusions: Genotype-phenotype correlations in patients with mutations affecting the genes that encode the electron input module of complex I vary, but patients with NDUFS1 mutation tend to have a worse clinical course than patients with NDUFV1 mutation. Identifying the mutations is of importance for accurate prognostic information and genetic counseling.
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9.
  • Lundin, Anna-Carin (författare)
  • Tendinosis in Trigger Finger
  • 2017
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • Trigger finger is one of the most common hand conditions, with a prevalence of almost 3%. The aetiology remains unclear even though many causes have been suggested. The prevailing paradigm is that the pathogenesis of trigger finger is ascribed to primary changes in the first fibrous condensation of the tendon sheath (A1-pulley). Several studies have investigated pathology in the pulley, but few have investigated the tendon. The general aim of this thesis was to find out if there is pathology in the trigger finger tendon and to define it.We first looked at trigger finger tendon biopsies in a light microscope, and found that they were histologically different from healthy tendons. They showed signs of micro-ruptures, collagen degradation, increased amounts of ground substance, both hyper- and hypo-cellular areas, round active cell nuclei and absence of inflammatory cells, all similar to tendinosis. The histological picture was further assessed by using a scoring system for Achilles tendinosis. The trigger finger tendons scored high, suggesting a similar histopathology.Next, we performed a quantitative real-time polymerase chain reaction (qPCR) on trigger finger tendons. We assessed the mRNA expression of 10 genes, which have been described to be differently expressed in Achilles tendinosis (collagen 1 and 3, versican, decorin, biglycan, aggrecan, MMP-2, MMP-3, ADAMTS-5, and TIMP-3). The overall expression pattern agreed with previous studies on Achilles tendinosis, suggesting that the cellular function in trigger finger tendons is disturbed in a similar way as in Achilles tendinosis.Recent experimental and observational research has suggested potential side effects of statin treatment on tendons, but firm evidence was lacking. We performed an epidemiological study on two large population-based cohorts. Statin use was found to increase the risk of both trigger finger and tendinosis in the shoulder and Achilles tendons, especially among men. This suggests a similar pathology in trigger finger and tendinosis.We have also studied the time to treatment effect after a single injection of glucocorticoid in trigger finger. Our results suggest that 60-80% of patients can expect resolution of the triggering within 14 days, and half of them within seven days. This result allows correct information to be given to the patient and proper planning of follow-ups.In conclusion, the pathology in trigger finger tendons is similar to tendinosis in other tendons.
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10.
  • Paterson, R W, et al. (författare)
  • A targeted proteomic multiplex CSF assay identifies increased malate dehydrogenase and other neurodegenerative biomarkers in individuals with Alzheimer's disease pathology.
  • 2016
  • Ingår i: Translational psychiatry. - : Springer Science and Business Media LLC. - 2158-3188. ; 6:11
  • Tidskriftsartikel (refereegranskat)abstract
    • Alzheimer's disease (AD) is the most common cause of dementia. Biomarkers are required to identify individuals in the preclinical phase, explain phenotypic diversity, measure progression and estimate prognosis. The development of assays to validate candidate biomarkers is costly and time-consuming. Targeted proteomics is an attractive means of quantifying novel proteins in cerebrospinal and other fluids, and has potential to help overcome this bottleneck in biomarker development. We used a previously validated multiplexed 10-min, targeted proteomic assay to assess 54 candidate cerebrospinal fluid (CSF) biomarkers in two independent cohorts comprising individuals with neurodegenerative dementias and healthy controls. Individuals were classified as 'AD' or 'non-AD' on the basis of their CSF T-tau and amyloid Aβ1-42 profile measured using enzyme-linked immunosorbent assay; biomarkers of interest were compared using univariate and multivariate analyses. In all, 35/31 individuals in Cohort 1 and 46/36 in Cohort 2 fulfilled criteria for AD/non-AD profile CSF, respectively. After adjustment for multiple comparisons, five proteins were elevated significantly in AD CSF compared with non-AD CSF in both cohorts: malate dehydrogenase; total APOE; chitinase-3-like protein 1 (YKL-40); osteopontin and cystatin C. In an independent multivariate orthogonal projection to latent structures discriminant analysis (OPLS-DA), these proteins were also identified as major contributors to the separation between AD and non-AD in both cohorts. Independent of CSF Aβ1-42 and tau, a combination of these biomarkers differentiated AD and non-AD with an area under curve (AUC)=0.88. This targeted proteomic multiple reaction monitoring (MRM)-based assay can simultaneously and rapidly measure multiple candidate CSF biomarkers. Applying this technique to AD we demonstrate differences in proteins involved in glucose metabolism and neuroinflammation that collectively have potential clinical diagnostic utility.
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