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Lindgren, Cecilia
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Lindgren, C., Koskinen, L.-O., Ssozi, R. & Naredi, S. (2019). Cerebrospinal fluid lactate and neurological outcome after subarachnoid haemorrhage. Journal of clinical neuroscience, 60, 63-67
Öppna denna publikation i ny flik eller fönster >>Cerebrospinal fluid lactate and neurological outcome after subarachnoid haemorrhage
2019 (Engelska)Ingår i: Journal of clinical neuroscience, ISSN 0967-5868, E-ISSN 1532-2653, Vol. 60, s. 63-67Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

BACKGROUND: Increased lactate in cerebrospinal fluid (CSF) has been regarded as a marker for cerebral ischemia and damage in the central nervous system. The aim of this study was to evaluate if CSF-lactate was associated with; impaired cerebral circulation, outcome, sex, age, clinical condition or treatment after subarachnoid haemorrhage (SAH).

METHODS: This study consists of 33 patients (22 females, 11 males) with aneurysmal SAH treated at Umeå university hospital 2008-2009. Samples were obtained from external ventricular catheters 0-240 h after SAH. Normal CFS-lactate was defined as 1.2-2-1 mmol/L. Hunt & Hess scale assessed clinical condition. Impaired cerebral circulation was evaluated by clinical examination, transcranial doppler, CT-scan, and cerebral angiography. Glasgow outcome scale (GOS) evaluated outcome.

RESULTS: Seventy-nine CSF-lactate samples were analysed. CSF-lactate >2.1 mmol/L was found in 25/33 (76%) patients and in 50/79 (63%) samples. No difference in CSF-lactate levels was found over time. No association was found between patients with CSF-lactate >2.1 mmol/L and; sex, severity of clinical condition, impaired cerebral circulation or outcome. CSF-lactate >2.1 mmol/L was more common in patients ≥61 years of age (p = 0.04) and in patients treated with endovascular coiling compared to surgical clipping (p = 0.0001).

CONCLUSION: In patients with SAH, no association was found between increased CSF-lactate (>2.1 mmol/L) and severe clinical condition, impaired cerebral circulation or unfavourable outcome. Endovascular coiling and age ≥61 years was associated with CSF-lactate above >2.1 mmol/L.

Ort, förlag, år, upplaga, sidor
Elsevier, 2019
Nyckelord
Cerebral aneurysms, Cerebrospinal fluid, Cerebrovascular circulation, Critical care outcomes, Endovascular procedures, Lactic acid
Nationell ämneskategori
Anestesi och intensivvård Kirurgi
Identifikatorer
urn:nbn:se:umu:diva-152935 (URN)10.1016/j.jocn.2018.10.025 (DOI)000456753600011 ()30361053 (PubMedID)
Forskningsfinansiär
Kempestiftelserna
Tillgänglig från: 2018-10-30 Skapad: 2018-10-30 Senast uppdaterad: 2019-02-26Bibliografiskt granskad
Lindgren, C., Naredi, S., Söderberg, S., Koskinen, L.-O. & Hultin, M. (2016). Leptin levels after subarachnoid haemorrhage are gender dependent. SpringerPlus, 5, Article ID 667.
Öppna denna publikation i ny flik eller fönster >>Leptin levels after subarachnoid haemorrhage are gender dependent
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2016 (Engelska)Ingår i: SpringerPlus, E-ISSN 2193-1801, Vol. 5, artikel-id 667Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Background: Subarachnoid hemorrhage (SAH) is a neurological disease where the majority of the patients are critically ill. The adipokine leptin has in cerebral emergencies been related to severity of disease and to adverse outcome. The aim of this study was to examine leptin levels over time after SAH and associations to gender, age, body mass index, severity of disease, parenteral lipids, systemic organ failure and outcome.

Methods: Prospective observational study in 56 patients. Leptin was obtained 0-240 h after SAH, in 48 h intervals. Severity of disease was assessed with the Hunt and Hess score, organ failure with the sequential organ failure assessment score, and outcome with Glasgow outcome scale. Leptin levels in the SAH group were compared with controls from the same geographical area.

Results: At admission, Leptin was significantly higher in SAH patients compared to controls, both in female (28.6 +/- 25.6 vs 13.0 +/- 2.3 ng/mL, p = 0.001) and male patients (13.3 +/- 8.4 vs 4.3 +/- 0.7 ng/mL, p = 0.001). Leptin levels remained stable over time. Female patients had significantly higher leptin levels than male patients, and deceased female patients had higher leptin levels than female survivors (85.5 +/- 20.5 vs 50.5 +/- 34.6, n = 4/35, p < 0.05). Leptin levels did not differ between male survivors and non-survivors. Leptin levels were not associated with severity of disease, organ failure or parenteral lipids.

Conclusion: Leptin levels were significantly higher in both male and female patients compared to controls. Higher leptin levels were related to outcome and organ failure in women but not in men. When analysing leptin levels gender-related differences should be considered.

Nyckelord
Leptin, Gender, Subarachnoid haemorrhage, Organ failure, Outcome
Nationell ämneskategori
Neurologi Anestesi och intensivvård
Identifikatorer
urn:nbn:se:umu:diva-123992 (URN)10.1186/s40064-016-2321-3 (DOI)000377611400001 ()27350906 (PubMedID)
Tillgänglig från: 2016-07-13 Skapad: 2016-07-07 Senast uppdaterad: 2018-06-07Bibliografiskt granskad
Sjöberg, R. L., Bergenheim, T., Mörén, L., Antti, H., Lindgren, C., Naredi, S. & Lindvall, P. (2015). Blood Metabolomic Predictors of 1-Year Outcome in Subarachnoid Hemorrhage. Neurocritical Care, 23(2), 225-232
Öppna denna publikation i ny flik eller fönster >>Blood Metabolomic Predictors of 1-Year Outcome in Subarachnoid Hemorrhage
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2015 (Engelska)Ingår i: Neurocritical Care, ISSN 1541-6933, E-ISSN 1556-0961, Vol. 23, nr 2, s. 225-232Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Delayed neurological deficit (DND) is the most important cause of morbidity and mortality in patients with subarachnoid hemorrhage (SAH) whose aneurysms have been secured. However, the methods currently used to predict the development of DND, such as trans-cranial Doppler or levels biochemical markers in blood and cerebrospinal fluid are not very accurate. Venous blood was drawn from 50 patients with SAH, admitted to the neurosurgical department UmeAyen University Hospital, at day 1-3 and day 7 after the bleed. The clinical status of the patients was followed up approximately 1 year after this episode and classified according to the Glasgow Outcome Score (GOS). Results showed considerable differences in blood metabolomic patterns between day 1-3 and 7 after the hemorrhage. Fifty-six out of 98 metabolites could be identified from our in-house library and 17 of these metabolites changed significantly from day 1-3 to 7 after the bleed. One of these, myo-inositol, was predictive of clinical outcome even after correction for multiple testing. An estimation of the diagnostic accuracy of high levels of this substance in predicting good outcome (GOS 4-5) yielded a sensitivity of .763 and a specificity of .5 at the optimal cut off point. SAH is an event with a profound effect on blood metabolomics profiles. Myo-inositol might be an interesting compound for future study to focus on in the search for metabolic markers in venous blood of delayed neurological deterioration in SAH patients.

Ort, förlag, år, upplaga, sidor
Springer, 2015
Nyckelord
Delayed neurological deficit, Myo-inositol, Metabolomics, Subarachnoid hemorrhage, Vasospasm, nous blood
Nationell ämneskategori
Neurovetenskaper
Identifikatorer
urn:nbn:se:umu:diva-109362 (URN)10.1007/s12028-014-0089-2 (DOI)000360700700012 ()25667130 (PubMedID)
Tillgänglig från: 2015-09-30 Skapad: 2015-09-25 Senast uppdaterad: 2018-06-07Bibliografiskt granskad
Lindgren, C., Söderberg, S., Koskinen, L.-O., Hultin, M., Edvardsson, L. & Naredi, S. (2015). Long-term subarachnoid haemorrhage survivors still die due to cerebrovascular causes. Acta Neurologica Scandinavica, 132(6), 410-416
Öppna denna publikation i ny flik eller fönster >>Long-term subarachnoid haemorrhage survivors still die due to cerebrovascular causes
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2015 (Engelska)Ingår i: Acta Neurologica Scandinavica, ISSN 0001-6314, E-ISSN 1600-0404, Vol. 132, nr 6, s. 410-416Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

OBJECTIVE: Subarachnoid haemorrhage (SAH) is associated with sympathetic nervous activation and inflammation. SAH could therefore theoretically be a risk factor for development of cardiovascular disease. The aim of this study was to investigate whether long-term (>/=1 year) SAH survivors had an increased risk of death due to cardiovascular causes. MATERIAL & METHODS: SAH patients >/=18 years treated at Umea University Hospital between 1986 and 2006 were eligible for inclusion. Deceased patients were identified in the Swedish population register. Death certificates from long-term SAH survivors and causes of death in the general population were obtained from the National Board of Health and Welfare, Sweden. The prevalence of comorbidities at the time of SAH was compared with the distribution of cardiovascular risk factors in the northern Sweden MONICA (Multinational Monitoring of Trends and Determinants in Cardiovascular Disease) health survey. Analyses were stratified for age and sex. RESULTS: In the SAH patients, the median year of SAH was 1992 and the median year of death was 2001. The MONICA survey in 1994 and the distribution of deaths in the general population in 2001 were used for comparison. Long-term SAH survivors had, compared to the general population, a significantly increased risk for death due to cerebrovascular disease (P < 0.0001), but not for death due to cardiovascular disease. Hypertension was more common in SAH patients compared to survey participants (P < 0.01). CONCLUSION: Cerebrovascular causes of death were significantly more common in long-term survivors after SAH compared to the general population.

Ort, förlag, år, upplaga, sidor
John Wiley & Sons, 2015
Nyckelord
cardiovascular disease, cerebrovascular disease, epidemiology, subarachnoid haemorrhage
Nationell ämneskategori
Anestesi och intensivvård Kirurgi
Identifikatorer
urn:nbn:se:umu:diva-102329 (URN)10.1111/ane.12410 (DOI)000362751600006 ()25864536 (PubMedID)1600-0404 (Electronic) 0001-6314 (Linking) (ISBN)
Tillgänglig från: 2015-04-23 Skapad: 2015-04-23 Senast uppdaterad: 2018-06-07Bibliografiskt granskad
Lindgren, C., Hultin, M., Koskinen, L.-O. D., Lindvall, P., Borota, L. & Naredi, S. (2014). ADMA levels and arginine/ADMA ratios reflect severity of disease and extent of inflammation after subarachnoid hemorraghe. Neurocritical Care, 21(1), 91-101
Öppna denna publikation i ny flik eller fönster >>ADMA levels and arginine/ADMA ratios reflect severity of disease and extent of inflammation after subarachnoid hemorraghe
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2014 (Engelska)Ingår i: Neurocritical Care, ISSN 1541-6933, E-ISSN 1556-0961, Vol. 21, nr 1, s. 91-101Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Background: Subarachnoid hemorrhage (SAH) is characterized by an inflammatory response that might induce endothelial dysfunction. The aim of this study was to evaluate if ADMA and arginine/ADMA ratios after SAH (indicators of endothelial dysfunction) are related to clinical parameters, inflammatory response, and outcome.

Methods: Prospective observational study. ADMA, arginine, C-reactive protein (CRP), and cytokines were obtained 0–240 h (h) after SAH. Definition of severe clinical condition was Hunt&Hess (H&H) 3–5 and less severe clinical condition H&H 1–2. Impaired cerebral circulation was assessed by clinical examination, transcranial doppler, CT-scan, and angiography. Glasgow outcome scale (GOS) evaluated the outcome.

Results: Compared to admission, 0–48 h after SAH, the following was observed 49–240 h after SAH; (a) ADMA was significantly increased at 97–240 h (highest 217–240 h), (b) CRP was significantly increased at 49–240 h (highest 73–96 h), (c) interleukin-6 (IL-6) was significantly lower at 97–240 h (highest 49–96 h), p < 0.05. ADMA, CRP, and IL-6 were significantly lower and peak arginine/ADMA ratio was significantly higher in patients with H&H 1–2 compared to patients with H&H 3–5, p < 0.05. The peak ADMA or the nadir arginine/ADMA ratio did not differ significantly between patients with (55 %) or without (45 %) signs of impaired cerebral circulation. The peak ADMA or the nadir arginine/ADMA ratio did not differ significantly between patients with GOS 1–3 and patients with GOS 4–5.

Conclusions: ADMA increased significantly after SAH, and the increase in ADMA started after the pro-inflammatory markers (CRP and IL-6) had peaked. This might indicate that endothelial dysfunction, with ADMA as a marker, is induced by a systemic inflammation.

Ort, förlag, år, upplaga, sidor
Humana Press, 2014
Nyckelord
ADMA, subarachnoid hemorrage, inflammation, interleukin
Nationell ämneskategori
Anestesi och intensivvård Neurovetenskaper Neurologi
Forskningsämne
anestesiologi
Identifikatorer
urn:nbn:se:umu:diva-87531 (URN)10.1007/s12028-013-9945-8 (DOI)000339350500014 ()24408146 (PubMedID)
Forskningsfinansiär
Svenska Sällskapet för Medicinsk Forskning (SSMF)
Tillgänglig från: 2014-04-02 Skapad: 2014-04-02 Senast uppdaterad: 2018-06-08Bibliografiskt granskad
Lindgren, C. (2014). Subarachnoid haemorrhage: clinical and epidemiological studies. (Doctoral dissertation). Umeå: Umeå universitet
Öppna denna publikation i ny flik eller fönster >>Subarachnoid haemorrhage: clinical and epidemiological studies
2014 (Engelska)Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
Abstract [en]

Background: Subarachnoid haemorrhage (SAH) is a severe stroke that in 85% of all cases is caused by the rupture of a cerebral aneurysm. The median age at onset is 50-55 years and the overall mortality is approximately 45%.Sufficient cortisol levels are important for survival. After SAH hypothalamic/pituitary blood flow may be hampered this could result in inadequate secretion of cortisol. SAH is also associated with a substantial inflammatory response. Asymmetric dimethyl arginine (ADMA), an endogenous inhibitor of nitric oxide synthase, mediates vasoconstriction and increased ADMA levels may be involved in inflammation and endothelial dysfunction. Continuous electroencephalogram (EEG) monitoring can be used to detect non-convulsive seizures, leading to ischemic insults in sedated SAH patients. Elevated ADMA levels are risk factors for vascular diseases. Vascular disease has been linked to stress, inflammation and endothelial dysfunction. SAH possesses all those clinical features and theoretically SAH could thus induce vascular disease.

Aims: 1. Assess cortisol levels after SAH, and evaluate associations between cortisol and clinical parameters. 2. Assess ADMA levels and arginine/ADMA ratios after SAH and evaluate associations between ADMA levels and arginine/ADMA ratios with severity of disease, co-morbidities, sex, age and clinical parameters. 3. Investigate occurrence of subclinical seizures in sedated SAH patients. 4. Evaluate if patients that survive a SAH ≥ one year have an increased risk of vascular causes of death compared to a normal population.

Results: Continuous infusion of sedative drugs was the strongest predictor for a low (<200 nmol/L) serum cortisol. The odds ratio for a sedated patient to have a serum cortisol < 200 nmol/L was 18.0 times higher compared to an un-sedated patient (p < 0.001). Compared to admission values, 0-48 hours after SAH, CRP increased significantly already in the time-interval 49-72 hours (p<0.05), peaked in the time-interval 97-120 hours after SAH and thereafter decreased. ADMA started to increase in the time-interval 97-120 hours (p<0.05). ADMA and CRP levels were significantly higher, and arginine/ADMA ratios were significantly lower in patients with a more severe condition (p<0.05). Epileptic seizure activity, in sedated SAH patients, was recorded in 2/28 (7.1%) patients during 5/5468 (0.09%) hours of continuous EEG monitoring. Cerebrovascular disease was significantly more common as a cause of death in patients that had survived a SAH ≥ one year, compared to the population from the same area (p<0.0001).

Conclusions: Continuous infusion of sedative drugs was associated with low (<200 nmol/L) cortisol levels. ADMA increased significantly after SAH, after CRP had peaked, indicating that endothelial dysfunction, with ADMA as a marker, is induced by a systemic inflammation. Patients with a more severe condition had significantly higher ADMA and CRP levels, and significantly lower arginine/ADMA ratio. Continuous sedation in sedated SAH patients seems to be beneficial in protecting from subclinical seizures. Cerebrovascular causes of death are more common in SAH survivors.

Ort, förlag, år, upplaga, sidor
Umeå: Umeå universitet, 2014. s. 74
Serie
Umeå University medical dissertations, ISSN 0346-6612 ; 1623
Nyckelord
Subarachnoid haemorrhage, ADMA, Cortisol, EEG, inflammation, epidemiology, endothelium, arginine
Nationell ämneskategori
Anestesi och intensivvård Neurovetenskaper
Forskningsämne
anestesiologi; neurokirurgi; epidemiologi
Identifikatorer
urn:nbn:se:umu:diva-87553 (URN)978-91-7459-791-2 (ISBN)
Disputation
2014-04-25, Sal D, T9, Norrlands universitetssjukhus, Umeå, 09:00 (Svenska)
Opponent
Handledare
Anmärkning

Funding: The Swedish Society of Medicine, the Faculty of Medicine at Umeå University, The Kempe Foundations and The Stroke Foundation of Northern Sweden supported this study financially.

Tillgänglig från: 2014-04-03 Skapad: 2014-04-02 Senast uppdaterad: 2018-06-08Bibliografiskt granskad
Lindgren, C., Dahlqvist, P., Lindvall, P., Nilsson, L., Koskinen, L.-O. & Naredi, S. (2013). Cortisol levels are influenced by sedation in the acute phase after subarachnoid haemorrhage. Acta Anaesthesiologica Scandinavica, 57(4), 452-460
Öppna denna publikation i ny flik eller fönster >>Cortisol levels are influenced by sedation in the acute phase after subarachnoid haemorrhage
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2013 (Engelska)Ingår i: Acta Anaesthesiologica Scandinavica, ISSN 0001-5172, E-ISSN 1399-6576, Vol. 57, nr 4, s. 452-460Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

BACKGROUND: Subarachnoid haemorrhage (SAH) is a life-threatening condition that may be aggravated by acute pituitary damage and cortisol insufficiency. Robust diagnostic criteria for critical illness-related corticosteroid insufficiency (CIRCI) are lacking. The aim of this study was to assess the frequency of CIRCI in the acute phase (0-240 h) after SAH and to evaluate associations between cortisol levels and clinical parameters (sedation, circulatory failure, gender, age, severity of disease, treatment). CIRCI was defined as a single morning serum cortisol (mSC) < 200 nmol/L. The lower limit for calculated free cortisol (cFC) was set at < 22 nmol/L, and for saliva cortisol at < 7.7 nmol/L.

METHODS: Fifty patients were included. Serum/saliva cortisol and corticosteroid-binding globulin were obtained every second morning. A logistic regression model was used for multivariate analysis comparing cortisol levels with clinical parameters.

RESULTS: Of the patients, 21/50 (42%) had an mSC < 200 nmol/L and 30/50 (60%) had a cFC < 22 nmol/L. In patients with continuous intravenous sedation, the odds ratio for a mSC to be < 200 nmol/L was 18 times higher (95% confidence interval 4.2-85.0, P < 0.001), and the odds ratio for a cFC to be < 22 nmol/L was 2.4 times higher (95% confidence interval 1.2-4.7, P < 0.05) compared with patients with no continuous intravenous sedation.

CONCLUSIONS: Continuous intravenous sedation was significantly associated with cortisol values under defined limits (mSC < 200, cFC < 22 nmol/L). The possibility that sedating drugs per se may influence cortisol levels should be taken into consideration before CIRCI is diagnosed.

Nationell ämneskategori
Anestesi och intensivvård
Identifikatorer
urn:nbn:se:umu:diva-64100 (URN)10.1111/aas.12014 (DOI)000316138800006 ()23167448 (PubMedID)
Tillgänglig från: 2013-01-15 Skapad: 2013-01-15 Senast uppdaterad: 2018-06-08Bibliografiskt granskad
Lindgren, C., Nordh, E., Naredi, S. & Olivecrona, M. (2012). Frequency of non-convulsive Seizures and non-convulsive status Epilepticus in Subarachnoid Hemorrhage patients in need of controlled ventilation and sedation. Neurocritical Care, 17(3), 367-373
Öppna denna publikation i ny flik eller fönster >>Frequency of non-convulsive Seizures and non-convulsive status Epilepticus in Subarachnoid Hemorrhage patients in need of controlled ventilation and sedation
2012 (Engelska)Ingår i: Neurocritical Care, ISSN 1541-6933, E-ISSN 1556-0961, Vol. 17, nr 3, s. 367-373Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

BACKGROUND: Non-convulsive seizures (NCSZ) can be more prevalent than previously recognized among comatose neuro-intensive care patients. The aim of this study was to evaluate the frequency of NCSZ and non-convulsive status epilepticus (NCSE) in sedated and ventilated subarachnoid hemorrhage (SAH) patients.

METHODS: Retrospective study at a university hospital neuro-intensive care unit, from January 2008 until June 2010. Patients were treated according to a local protocol, and were initially sedated with midazolam or propofol or combinations of these sedative agents. Thiopental was added for treatment of intracranial hypertension. No wake-up tests were performed. Using NicoletOne((R)) equipment (VIASYS Healthcare Inc., USA), continuous EEG recordings based on four electrodes and a reference electrode was inspected at full length both in a two electrode bipolar and a four-channel referential montage.

RESULTS: Approximately 5,500 h of continuous EEG were registered in 28 SAH patients (33 % of the patients eligible for inclusion). The median Glasgow Coma scale was 8 (range 3-14) and the median Hunt and Hess score was 4 (range 1-4). During EEG registration, no clinical seizures were observed. In none of the patients inter ictal epileptiform activity was seen. EEG seizures were recorded only in 2/28 (7 %) patients. One of the patients experienced 4 min of an NCSZ and one had a 5 h episode of an NCSE.

CONCLUSION: Continuous EEG monitoring is important in detecting NCSZ in sedated patients. Continuous sedation, without wake-up tests, was associated with a low frequency of subclinical seizures in SAH patients in need of controlled ventilation.

Ort, förlag, år, upplaga, sidor
Totowa, NJ, USA: Humana Press, 2012
Nyckelord
Epilepsy, Seizures, Non-convulsive seizures, Continuous electroencephalogram, Subarachnoid hemorrhage
Nationell ämneskategori
Anestesi och intensivvård
Identifikatorer
urn:nbn:se:umu:diva-59419 (URN)10.1007/s12028-012-9771-4 (DOI)1556-0961 (Electronic) 1541-6933 (Linking) (ISBN)
Tillgänglig från: 2012-09-13 Skapad: 2012-09-13 Senast uppdaterad: 2018-06-08Bibliografiskt granskad
Lindgren, C., Hultin, M., Koskinen, L.-O., Söderberg, S., Edvardsson, L. & Naredi, S.Long term survivors of subarachnoid haemorrhage have an increased risk of death due to cerebrovascular causes.
Öppna denna publikation i ny flik eller fönster >>Long term survivors of subarachnoid haemorrhage have an increased risk of death due to cerebrovascular causes
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(Engelska)Manuskript (preprint) (Övrigt vetenskapligt)
Nyckelord
epidemiology, subarachnoid haemorrhage, cerebrovascular disease, cardiovascular disease
Nationell ämneskategori
Anestesi och intensivvård
Forskningsämne
epidemiologi
Identifikatorer
urn:nbn:se:umu:diva-87551 (URN)
Tillgänglig från: 2014-04-02 Skapad: 2014-04-02 Senast uppdaterad: 2018-06-08Bibliografiskt granskad
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