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Träfflista för sökning "WFRF:(Nylén Karin 1961) "

Search: WFRF:(Nylén Karin 1961)

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1.
  • Csajbok, Ludvig Z, 1964, et al. (author)
  • Apolipoprotein E polymorphism in aneurysmal subarachnoid haemorrhage in West Sweden.
  • 2016
  • In: Acta neurologica Scandinavica. - : Hindawi Limited. - 1600-0404 .- 0001-6314. ; 133:6, s. 466-474
  • Journal article (peer-reviewed)abstract
    • Aneurysmal subarachnoid haemorrhage (aSAH) is associated with high morbidity and mortality despite novel treatments. Genetic variability may explain outcome differences. Apolipoprotein E (ApoE) is a glycoprotein with a major role in brain lipoprotein metabolism. It has three isoforms encoded by distinct alleles: APOEε2, APOEε3 and APOEε4. The APOEε4 allele is associated with Alzheimer's disease and worse outcome after traumatic brain injury and ischaemic stroke. This prospective blinded study explored the influence of the APOEε4 polymorphism on the risk of aSAH, risk of cerebral vasospasm (CVS) and 1-year neurological outcome.
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4.
  • Ladenvall, Claes, 1974, et al. (author)
  • Association between factor XIII single nucleotide polymorphisms and aneurysmal subarachnoid hemorrhage Clinical article
  • 2009
  • In: JOURNAL OF NEUROSURGERY. - 0022-3085. ; 110:3, s. 475-481
  • Journal article (peer-reviewed)abstract
    • Object Family studies have suggested a role of genetic factors in susceptibility to aneurysmal subarachnoid hemorrhage (aSAH), but the underlying genetic risk factors remain poorly defined. There is an activation of the fibrinolytic system in aSAH, and fibrinolytic markers may be useful in predicting outcome. The authors investigate associations between putative functional variants in genes of importance for fibrinolysis and aSAH and/or outcome following aSAH. Methods One hundred eighty-three patients presenting with aSAH at a neurointensive care unit were consecutively recruited. Two healthy controls per case, matched for age, sex, and geographic region, were randomly recruited. Outcome was assessed after 1 year according to the extended Glasgow Outcome Scale. Single nucleotide polymorphisms (SNPs) in the tissue-type plasminogen activator (tPA), plasminogen activator inhibitor type 1 (PAI-1), thrombin activatable fibrinolysis inhibitor (TAFI), and factor XIII (FXIII) genes were investigated. Results Participants carrying the FXIII 34Leu allele showed an increased risk of aSAH. When adjusting for smoking and hypertension, 2 haplotypes, differing on either the FXIII Val34Leu or the Pro564Leu position, showed an association to aSAH. No significant association was observed for the tPA -7351 C > T, PAI-1 -675 4G > 5G, or TAFI Ala147Thr SNPs. No specific SNP or haplotype was associated with outcome after aSAH, whereas a weak association was observed for a tPA/PAI-1 genotype combination. Conclusions Polymorphisms in the FXIII gene showed association to aSAH. The finding of an increased risk of bleeding in FXIII 34Leu carriers is biologically plausible.
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5.
  • Lönnbro, Johan, et al. (author)
  • Developing professional confidence in the art of prescribing-a randomized controlled study on structured collegial discussions during internship.
  • 2019
  • In: European journal of clinical pharmacology. - : Springer Science and Business Media LLC. - 1432-1041 .- 0031-6970. ; 75:5, s. 687-696
  • Journal article (peer-reviewed)abstract
    • To evaluate whether an educational intervention based on collegial discussions on patient cases could increase interns' professional confidence in prescribing.In a randomized controlled study at Sahlgrenska University Hospital, Gothenburg, Sweden, 69 interns (median age: 29years, 54% female) were allocated to an intervention or control group. The intervention consisted of two 3-h seminars based on collegial discussions of patient cases focused on performing medication reviews. This included reconciling the drug treatment and ascertaining that it is reasonable given the patient's current health status, as well as tips on practical handling of the medical records system and integrated decision support. Self-assessed confidence in performing medication reviews was evaluated with questionnaires distributed at baseline and at 6-month follow-up.Fifty-seven (83%) interns completed the questionnaires. Although the opposite was found at baseline, intervention interns, in comparison with controls, at follow-up, were more confident in performing medication reviews (4.3±0.9 vs. 3.6±1.3, P=0.034; 1=completely disagree to 5=completely agree). At follow-up, the intervention participants had increased their confidence in prescribing to a greater extent compared with the control participants, including performing medication reviews as well as taking responsibility for the medication list at discharge: +1.5/+1 vs ±0 on the 5-point agreement scale (all P≤0.01). Among other positive outcomes, the intervention increased the interns' awareness of adverse effects as a potential cause of symptoms and their confidence in withdrawing a medication.Structured collegial discussions on pharmacotherapy, even of a relatively short duration, can increase junior physicians' professional confidence in prescribing medicines.
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6.
  • Nylén, Karin, 1961, et al. (author)
  • CSF -neurofilament correlates with outcome after aneurysmal subarachnoid hemorrhage.
  • 2006
  • In: Neurosci Lett. - : Elsevier BV. - 0304-3940. ; 404:1-2, s. 132-6
  • Journal article (peer-reviewed)abstract
    • Aneurysmal subarachnoid hemorrhage (aSAH) is a devastating event. Following the bleeding, a number of pathophysiological changes and clinical factors determine outcome. Not surprisingly, attempts to predict outcome based on a single factor have failed. The neurological status graded at admission to hospital and distributions of the blood on CT are the strongest predictors. There is evidence that cerebrospinal fluid (CSF) proteins may serve as markers of the extent of brain damage. The present study is focused on the light unit of neurofilament protein (NFL), previously not evaluated in aSAH. Lumbar puncture (LP), neurological grading according to World Federation of Neurological Surgeons (WFNS) and neurological examination according to the National Institute of Health Stroke Scale (NIHSS) were performed in 48 consecutive patients with aSAH 10-14 days after the hemorrhage. CSF-NFL concentrations were analyzed using an ELISA. Outcome was assessed after 1 year and categorised according to the extended Glasgow Outcome Scale (GOSE). A significant correlation between CSF-NFL and GOSE was detected at follow up after 1 year. CSF-NFL also correlated with WFNS and NIHSS on the day of the lumbar puncture. CSF-NFL is a biochemical marker of brain damage correlating to neurological status and long-term outcome after aneurysmal subarachnoid hemorrhage.
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7.
  • Nylén, Karin, 1961, et al. (author)
  • Serum glial fibrillary acidic protein is related to focal brain injury and outcome after aneurysmal subarachnoid hemorrhage.
  • 2007
  • In: Stroke. - 1524-4628. ; 38:5, s. 1489-94
  • Journal article (peer-reviewed)abstract
    • BACKGROUND AND PURPOSE: Aneurysmal subarachnoid hemorrhage (aSAH) stands out from other subtypes of stroke because of the high early mortality and the risk of complications. Serum glial fibrillary acidic protein (s-GFAP) concentrations are increased after stroke. The aim of this study was to investigate whether s-GFAP could be used as a marker of brain damage and outcome after aSAH. METHODS: Serum samples were obtained on a regular basis from 116 adults during a 2-week period after aSAH and analyzed using an enzyme-linked immunosorbent assay. The World Federation of Neurological Surgeons scale was used for neurological evaluation. Outcome was assessed after 1 year and categorized according to the Extended Glasgow Outcome Scale. RESULTS: Increased s-GFAP levels were seen in 81 of the 116 patients. Maximum s-GFAP correlated with World Federation of Neurological Surgeons scale on arrival and on days 10 to 15 (r=0.37, P<0.001 and r=0.47, P<0.001, respectively). Furthermore, maximum s-GFAP levels were increased in the patient group with radiological signs of focal lesions acute or at 1 year, compared with the group without focal lesions (P<0.001 in both comparisons). Patients with secondary events (re-bleeding or ischemia) reached maximum levels later in the series and both maximum and final s-GFAP levels increased compared with the levels in patients without secondary events (P<0.001 in all 3 comparisons). Finally, maximum s-GFAP correlated with outcome (r=-0.48, P<0.001) and s-GFAP was an independent predictor of dichotomized outcome. CONCLUSIONS: s-GFAP provides information about brain injury severity and outcome after aSAH, which can be useful as a complement to clinical data.
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8.
  • Nylén, Karin, 1961, et al. (author)
  • Serum levels of S100B, S100A1B and S100BB are all related to outcome after severe traumatic brain injury.
  • 2008
  • In: Acta neurochirurgica. - : Springer Science and Business Media LLC. - 0942-0940 .- 0001-6268. ; 150:3
  • Journal article (peer-reviewed)abstract
    • OBJECTIVES: S100B is an established marker of brain damage. Used in the context as a biochemical marker, S100B denotes a measurement of all S100 proteins, including at least one S100B monomer, i.e. the sum of the two dimers S100A1B and S100BB. Almost all published studies are based on this "sum concentration". However, the brain specificity of S100B has been questioned and increased serum levels have also been reported after trauma without head injury. Since the S100B monomer dominates in the brain, we hypothesised that the S100BB dimer should be better related to outcome after severe traumatic brain injury than S100A1B or the "sum concentration". METHODS: Daily serum samples were collected from 59 patients with severe traumatic brain injury. Three different ELISA methods were used for measurements of S100B, S100A1B and S100BB respectively. Outcome was assessed after one year and categorised according to the Glasgow Outcome Scale. RESULTS: Serum levels of S100B, S100A1B and S100BB followed the same temporal course, with early maximum and rapidly decreasing values over the first days after the trauma. Maximum serum concentrations of each of the parameters were increased in the patient group with an unfavourable outcome compared with those with a favourable outcome (p = 0.01, 0.006 and 0.004, respectively). CONCLUSION: Both S100A1B and S100BB were related to outcome after severe traumatic brain injury. Even though this study is small, it seems unlikely that separate analyses of the dimers are of any advantage compared with measuring S100B alone.
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9.
  • Nylén, Karin, 1961 (author)
  • Studies of biochemical brain damage markers in patients at a neurointensive care unit
  • 2007
  • Doctoral thesis (other academic/artistic)abstract
    • Physical examination is the basic and most important tool in medical practice. However, at a neurointensive care unit, neurological status can sometimes be difficult to evaluate due to sedation or impaired consciousness. Repeated radiology may not always be feasible. The aims of the present study were to investigate whether Glial Fibrillary Acidic Protein (GFAP) measured in serum could be used as a biochemical brain damage marker. To investigate whether concentrations of CSF-NFL were associated with brain injury severity and long-term outcome after aneurysmal subarachnoid haemorrhage (aSAH). Finally, to compare the two dimers S100A1B and S100BB with S100B, when it came to outcome after severe traumatic brain injury (TBI). Serum samples were obtained on a regular basis from 116 patients with aSAH and 59 patients with TBI during a two-week period. LP was performed in a subgroup of patients (n=48) with aSAH. The concentrations of the markers were analysed using ELISA methods. Clinical and radiological findings were estimated in the acute phase and outcome was assessed after one year using the Glasgow Outcome Scale. After aSAH maximum s-GFAP was increased in 81 of the patients and was normal in 35. A normal concentration predicted a favourable outcome. Increased s-GFAP levels were related to focal brain lesions, neurological complications and poor outcome. The concentrations of CSF-NFL were related to focal brain injury and outcome after aSAH. After severe TBI maximum s-GFAP was increased in all but one of the patients. The five patients with the most pronounced increase died. The serum concentrations of GFAP, S100B, S100A1B and S100BB were all related to outcome. We conclude that s-GFAP can be used as a biochemical brain damage marker after aSAH and severe TBI. The high npv (32/35) after aSAH is the main finding, which may provide information to complement clinical data. CSF-NFL is a sensitive brain damage marker after aSAH, but for better utility, an analysis method for serum is needed. In the clinical setting in this study the investigated serum markers (GFAP, S100B, S100A1B, S100BB) appeared to predict outcome after severe TBI equally well.
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10.
  • Olsson, Annika, et al. (author)
  • Marked increase of beta-amyloid(1-42) and amyloid precursor protein in ventricular cerebrospinal fluid after severe traumatic brain injury.
  • 2004
  • In: Journal of neurology. - : Springer Science and Business Media LLC. - 0340-5354 .- 1432-1459. ; 251:7, s. 870-6
  • Journal article (peer-reviewed)abstract
    • Severe traumatic brain injury (TBI) may result in widespread damage to axons, termed diffuse axonal injury. Alzheimer's disease (AD) is characterised by synaptic and axonal degeneration together with senile plaques (SP). SP are mainly composed of aggregated beta-amyloid (Abeta), which are peptides derived from the amyloid precursor protein (APP). Apart from TBI in itself being considered a risk factor for AD, severe head injury seems to initiate a cascade of molecular events that are also associated with AD. We have therefore analysed the 42 amino acid forms of Abeta (Abeta1-42) and two soluble forms of APP (alpha-sAPP and ss-sAPP) in ventricular cerebrospinal fluid (VCSF) and Abeta(1-42) in plasma from 28 patients in a serial samples 0-11 days after TBI. The levels of alpha-sAPP, ss-sAPP and Abeta(1-42) were determined using ELISA assays. After TBI, there was a significant stepwise increase in VCSF-Abeta(1-42) up to 1173 % from day 0-1 to day 5-6 and in VCSF-beta-sAPP up to 2033 % increase from day 0-1 to day 7-11. There was also a slight but significant increase of VCSF-beta-sAPP from day 0-1 to day 5-6 and day 7-11. By contrast, the plasma- Abeta(1-42) level is unchanged after injury. The marked increase in VCSFAbeta(1-42) implies that increased Abeta expression may occur as a secondary phenomenon after TBI with axonal damage. The unchanged level of plasma-Abeta(1-42) in contrast to the marked increase in VCSF-Abeta(1-42) after severe TBI, supports the suggestion that plasma Abeta(1-42) does not reflect Abeta metabolism in the central nervous system (CNS).
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