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Sökning: WFRF:(Lindvall Bo)

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1.
  • Bartek, Jiri, Jr., et al. (författare)
  • Scandinavian Multicenter Acute Subdural Hematoma (SMASH) Study : Study Protocol for a Multinational Population-Based Consecutive Cohort
  • 2019
  • Ingår i: Neurosurgery. - : Ovid Technologies (Wolters Kluwer Health). - 0148-396X .- 1524-4040. ; 84:3, s. 799-803
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUNDTraumatic acute subdural hematomas (ASDHs) are associated with high rate of morbidity and mortality, especially in elderly individuals. However, recent reports indicate that the morbidity and mortality rates might have improved.OBJECTIVETo evaluate postoperative (30-d) mortality in younger vs elderly (70 yr) patients with ASDH. Comparing younger and elderly patients, the secondary objectives are morbidity patterns of care and 6 mo outcome according to Glasgow outcome scale (GOS). Finally, in patients with traumatic ASDH, we aim to provide prognostic variables.METHODS This is a large-scale population-based Scandinavian study including all neurosurgical departments in Denmark and Sweden. All adult (18 yr) patients surgically treated between 2010 and 2014 for a traumatic ASDH in Denmark and Sweden will be included. Identification at clinicaltrials.gov is NCT03284190.EXPECTED OUTCOMESWe expect to provide data on potential differences between younger vs elderly patients in terms of mortality and morbidity. We hypothesize that elderly patients selected for surgery have a similar pattern of care as compared with younger patients. We will provide functional outcome in terms of GOS at 6 mo in younger vs elderly patients undergoing ASDH evacuation. Finally, clinical useful prognostic factors for favorable (GOS 4-5) vs unfavorable (GOS 1-3) will be identified.DISCUSSION An improved understanding of the clinical outcome, treatment and resource allocation, clinical course, and the prognostic factors of traumatic ASDH will allow neurosurgeons to make better treatment decisions.
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  • Erlinge, D., et al. (författare)
  • Bivalirudin versus Heparin Monotherapy in Myocardial Infarction
  • 2017
  • Ingår i: New England Journal of Medicine. - : Massachusetts Medical Society. - 0028-4793 .- 1533-4406. ; 377:12, s. 1132-1142
  • Tidskriftsartikel (refereegranskat)abstract
    • Background The comparative efficacy of various anticoagulation strategies has not been clearly established in patients with acute myocardial infarction who are undergoing percutaneous coronary intervention (PCI) according to current practice, which includes the use of radial-artery access for PCI and administration of potent P2Y12 inhibitors without the planned use of glycoprotein IIb/IIIa inhibitors. Methods In this multicenter, randomized, registry-based, open-label clinical trial, we enrolled patients with either ST-segment elevation myocardial infarction (STEMI) or non-STEMI (NSTEMI) who were undergoing PCI and receiving treatment with a potent P2Y12 inhibitor (ticagrelor, prasugrel, or cangrelor) without the planned use of glycoprotein IIb/IIIa inhibitors. The patients were randomly assigned to receive bivalirudin or heparin during PCI, which was performed predominantly with the use of radial-artery access. The primary end point was a composite of death from any cause, myocardial infarction, or major bleeding during 180 days of follow-up. Results A total of 6006 patients (3005 with STEMI and 3001 with NSTEMI) were enrolled in the trial. At 180 days, a primary end-point event had occurred in 12.3% of the patients (369 of 3004) in the bivalirudin group and in 12.8% (383 of 3002) in the heparin group (hazard ratio, 0.96; 95% confidence interval [CI], 0.83 to 1.10; P=0.54). The results were consistent between patients with STEMI and those with NSTEMI and across other major subgroups. Myocardial infarction occurred in 2.0% of the patients in the bivalirudin group and in 2.4% in the heparin group (hazard ratio, 0.84; 95% CI, 0.60 to 1.19; P=0.33), major bleeding in 8.6% and 8.6%, respectively (hazard ratio, 1.00; 95% CI, 0.84 to 1.19; P=0.98), definite stent thrombosis in 0.4% and 0.7%, respectively (hazard ratio, 0.54; 95% CI, 0.27 to 1.10; P=0.09), and death in 2.9% and 2.8%, respectively (hazard ratio, 1.05; 95% CI, 0.78 to 1.41; P=0.76). Conclusions Among patients undergoing PCI for myocardial infarction, the rate of the composite of death from any cause, myocardial infarction, or major bleeding was not lower among those who received bivalirudin than among those who received heparin monotherapy. (Funded by the Swedish Heart-Lung Foundation and others; VALIDATE-SWEDEHEART ClinicalTrialsRegister.eu number, 2012-005260-10 ; ClinicalTrials.gov number, NCT02311231 .).
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  • Aked, Joseph, et al. (författare)
  • Attitudes to Stem Cell Therapy among Ischemic Stroke Survivors in the Lund Stroke Recovery Study
  • 2017
  • Ingår i: Stem Cells and Development. - : Mary Ann Liebert Inc. - 1547-3287 .- 1557-8534. ; 26:8, s. 566-572
  • Tidskriftsartikel (refereegranskat)abstract
    • Preclinical studies suggest that stem cell therapy (SCT) may improve poststroke recovery, and clinical trials investigating safety are ongoing. However, knowledge about patients' attitudes to SCT in stroke is limited. We evaluated the knowledge and attitudes to this therapeutic approach as well as possible factors influencing this among stroke patients potentially suitable for SCT. Consecutive first-ever acute ischemic stroke patients aged 20-75 years with NIH stroke scale scores 1-18 were included. Exclusion criteria were severe comorbidities or infratentorial stroke. Clinical follow-up after 3-5 years assessed severity of residual stroke symptoms, cognitive function, functional status, patient-reported outcome, and comorbidity, and after receiving standardized information, the participants also completed an eight-item questionnaire on knowledge and attitudes about SCT. The relationships between clinical variables and positive attitude to SCT were assessed with logistic regression analyses. Of 108 patients included at baseline, 84 participated at follow-up and completed the questionnaire. In total, 12% had prior knowledge of SCT. When informed, 63% were positive toward it and 36% reported willingness to participate in SCT trials. Only 5%-8% expressed ethical considerations regarding different stem cell sources. Positive attitudes to SCT were associated with male gender (OR: 3.74; 95% CI: 1.45-9.61; P < 0.01) and better patient-reported outcome (OR: 1.02; 95% CI: 1.00-1.04; P < 0.05). In conclusion, stroke patients had limited prior knowledge of SCT, yet attitudes were positive among the majority after receiving standardized and neutral information. Gender and degree of stroke recovery may influence attitudes to SCT, indicating a need for targeted information to improve knowledge about SCT.
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  • Dahlström, Carl, 1972, et al. (författare)
  • Corruption, Bureaucratic Failure and Social Policy Priorities
  • 2013
  • Ingår i: Political Studies. - : SAGE Publications. - 0032-3217 .- 1467-9248. ; 61:3, s. 523-542
  • Tidskriftsartikel (refereegranskat)abstract
    • This article argues that bureaucratic capacity - the competence and reliability of the national bureaucracy - matters to the allocation of public spending among welfare state programmes since it is difficult for governments to justify high levels of spending on programmes that require bureaucrats to make case-by-case decisions, on a discretionary basis, if the bureaucracy is incompetent, corrupt or both. We expect bureaucratic capacity to have a positive effect on programmes that involve bureaucratic discretion, but weak or no effects on programmes that are more straightforward to implement. In order to test these hypotheses, we analyse public spending on active labour market programmes (which involve a lot of discretion) and parental leave benefits (which involve less discretion). Relying on data for twenty advanced democracies from the mid-1980s to the mid-2000s, we find that high bureaucratic capacity does have a positive effect on active labour market policy spending, but not on parental leave benefits.
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  • Delavaran, Hossein, et al. (författare)
  • Proximity of brain infarcts to regions of endogenous neurogenesis and involvement of striatum in ischaemic stroke.
  • 2012
  • Ingår i: European Journal of Neurology. - : Wiley. - 1351-5101 .- 1468-1331.
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Clinical stroke trials with stem cell-based approaches aiming for trophic actions, modulation of inflammation and neuroprotection are ongoing. However, experimental studies also suggest that neuronal replacement by grafted neural stem cells (NSCs) and possibly by endogenous NSCs from the subventricular zone (SVZ) may restore function in the stroke-damaged striatum. To evaluate the potential clinical impact of these findings, we analyzed the spatial relationship of infarcts to the SVZ and the proportion of individuals with striatal lesions in a consecutive series of ischaemic stroke patients. METHODS: Patients aged 20-75 years with first-ever ischaemic stroke underwent DW-MRI of the brain within 4 days after stroke onset. We analyzed location, size, number of acute focal ischaemic abnormalities and their spatial relationship to the SVZ. Stroke severity was assessed using NIH Stroke Scale (NIHSS). RESULTS: Of 108 included patients, the distance from the nearest margin of the infarct(s) to the SVZ was ≤2 mm in 51/102 patients with visible ischaemic lesions on DW-MRI. Twenty-four patients had involvement of striatum. Eight of these had predominantly striatal lesions, that is >50% of the total ischaemic lesion volume was located in caudate nucleus and/or putamen. These 8 patients had a median NIHSS of 3. CONCLUSIONS: Many stroke patients have infarcts located close to the SVZ, providing some supportive evidence that optimized endogenous neurogenesis may have therapeutic potential. However, predominantly striatal infarcts are rare and tend to give mild neurological deficits, indicating that striatum should not be the primary target for neuronal replacement efforts in humans.
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8.
  • Delavaran, Hossein, et al. (författare)
  • Spontaneous Recovery of Upper Extremity Motor Impairment After Ischemic Stroke : Implications for Stem Cell-Based Therapeutic Approaches
  • 2017
  • Ingår i: Translational Stroke Research. - : Springer Science and Business Media LLC. - 1868-4483 .- 1868-601X. ; 8:4, s. 351-361
  • Tidskriftsartikel (refereegranskat)abstract
    • Preclinical studies suggest that stem cell therapy (SCT) may improve sensorimotor recovery after stroke. Upper extremity motor impairment (UEMI) is common after stroke, often entailing substantial disability. To evaluate the feasibility of post-stroke UEMI as a target for SCT, we examined a selected sample of stroke patients potentially suitable for SCT, aiming to assess the frequency and recovery of UEMI, as well as its relation to activity limitations and participation restrictions. Patients aged 20–75 years with first-ever ischemic stroke, and National Institutes of Health Stroke Scale (NIHSS) scores 1–18, underwent brain diffusion-weighted MRI within 4 days of stroke onset (n = 108). Survivors were followed up after 3–5 years, including assessment with NIHSS, Fugl-Meyer assessment of upper extremity (FMA-UE), modified Rankin Scale (mRS), and Stroke Impact Scale (SIS). UEMI was defined as NIHSS arm/hand score ≥1. UEMI recovery was evaluated with change in NIHSS arm/hand scores between baseline and follow-up. Of 97 survivors, 84 were available to follow-up. Among 76 subjects (of 84) without recurrent stroke, 41 had UEMI at baseline of which 10 had residual UEMI at follow-up. The FMA-UE showed moderate-severe impairment in seven of 10 survivors with residual UEMI. UEMI was correlated to mRS (rs = 0.49, p < 0.001) and the SIS social participation domain (rs = −0.38, p = 0.001). Nearly 25% of the subjects with UEMI at baseline had residual impairment after 3–5 years, whereas about 75% showed complete recovery. Most of the subjects with residual UEMI had moderate-severe impairment, which correlated strongly to dependency in daily activities and social participation restrictions. Our findings suggest that SCT targeting post-stroke UEMI may be clinically valuable with significant meaningful benefits for patients but also emphasize the need of early prognostication to detect patients that will have residual impairment in order to optimize patient selection for SCT.
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  • Johansson, Niklas (författare)
  • Self-Service Recovery
  • 2007
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • Service recovery is about problems. What happens when customers experience problems? Well, sometimes customers complain to the one responsible for the service. Sometimes customers do not complain but instead tell somebody else about the problem, possibly leading to a bad reputation for the one responsible for the service. Sometimes it happens that customers never return to the same provider because of the problem experienced. To avoid the customer leaving, service recovery can be used. Service recovery is a set of actions a service pro-vider can take in order to repair a failure (Tax and Brown, 1998; Zemke, 1995; Scheuing and Christopher, 1993; Levesque and McDougall, 2000).In addition, many services today are Internet-based, meaning that services are self-services enabled by information technology (IT). Self-services enabled by IT, referred to as self-service technology (SST), are characterized by an interac-tion between a user and a machine rather than between two humans. Conse-quently, service recovery is no longer between two people interacting in a face-to-face manner when solving problems, but between a user and a machine when taking place in an SST context.This change of context has resulted in difficulties but also opportunities in the work of service recovery. Instead of turning to the one responsible for the service when problems occur, it is now possible to turn to other customers and users to receive help. SST has opened up new opportunities to learn with and from other individuals through the sharing of knowledge. The sharing of knowledge for the purpose of turning problems into solutions and improve-ments depends on the ability to create value for people involved.Service recovery in a self-service technology context, i.e. self-service recovery (SSR) is defined as the capability, enabled by self-service technology, of turning user prob-lems into solutions and improvements by means of sharing knowledge between users in order to create value.The aim of this doctoral thesis is to answer the question, “Why self-service recovery works?” The question is addressed by seven research studies and by evolving a framework for understanding why self-service recovery works.The contributions of this dissertation reside from the framework, which en-hances our understanding of self-service recovery as a value creation activity through not only recovery, but also improvement of the service in question.
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  • Kokaia, Zaal, et al. (författare)
  • Brain insults in rats induce increased expression of the BDNF gene through differential use of multiple promoters
  • 1994
  • Ingår i: European Journal of Neuroscience. - : Wiley. - 1460-9568 .- 0953-816X. ; 6:4, s. 587-596
  • Tidskriftsartikel (refereegranskat)abstract
    • The rat brain-derived neurotrophic factor (BDNF) gene consists of four short 5'-exons linked to separate promoters and one 3'-exon encoding the mature BDNF protein. Using in situ hybridization we demonstrate here that kindling-induced seizures, cerebral ischaemia and insulin-induced hypoglycaemic coma increase BDNF mRNA levels through insult- and region-specific usage of three promoters within the BDNF gene. Both brief (2 min) and longer (10 min) periods of forebrain ischaemia induced significant and major increases only of exon III mRNA in the dentate gyrus. Following hypoglycaemic coma (1 and 30 min), exon III mRNA was markedly elevated in the dentate gyrus and, in addition, exon I mRNA showed a moderate increase. Single and recurrent (n = 40) hippocampal seizures significantly increased expression of exon I, II and III mRNAs in the dentate gyrus granule cells. After recurrent seizures, including generalized convulsions, there were also major increases of both exon I and III mRNAs in the CA3 region, amygdala, piriform cortex and neocortex, whereas in the hippocampal CA1 sector marked elevations were detected only for exon III mRNA. The insults had no effect on the level of exon IV mRNA in the brain. The region- and insult-specific pattern of promoter activation might be of importance for the effectiveness of protective responses as well as for the regulation of plastic changes following brain insults.
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  • Kokaia, Zaal, et al. (författare)
  • Regulation of brain-derived neurotrophic factor gene expression after transient middle cerebral artery occlusion with and without brain damage
  • 1995
  • Ingår i: Experimental Neurology. - : Elsevier BV. - 0014-4886. ; 136:1, s. 73-88
  • Tidskriftsartikel (refereegranskat)abstract
    • Levels of mRNA for c-fos, nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), TrkB, and TrkC were studied using in situ hybridization in the rat brain at different reperfusion times after unilateral middle cerebral artery occlusion (MCAO). Short-term (15 min) MCAO, which does not cause neuronal death, induced elevated BDNF mRNA expression confined to ipsilateral frontal and cingulate cortices outside the ischemic area. With a longer duration of MCAO (2 h), which leads to cortical infarction, the increase was more marked and elevated BDNF mRNA levels were also detected bilaterally in dentate granule cells and CA1 and CA3 pyramidal neurons. Maximum expression was found after 2 h of reperfusion. At 24 h BDNF mRNA expression had returned to control values. In the ischemic core of the parietal cortex only scattered neurons were expressing high levels of BDNF mRNA after 15 min and 2 h of MCAO. Analysis of different BDNF transcripts showed that MCAO induced a marked increase of exon III mRNA but only small increases of exon I and II mRNAs in cortex and hippocampus. In contrast to BDNF mRNA, elevated expression of c-fos mRNA was observed in the entire ipsilateral cerebral cortex, including the ischemic core, after both 15 min and 2 h of MCAO. Two hours of MCAO also induced transient, bilateral increases of NGF and TrkB mRNA levels and a decrease of NT-3 mRNA expression, confined to dentate granule cells. The upregulation of BDNF mRNA expression in cortical neurons after MCAO is probably triggered by glutamate through a spreading depression-like mechanism. The lack of response of the BDNF gene in the ischemic core may be due to suppression of signal transduction or transcription factor synthesis caused by the ischemia. The observed pattern of gene expression after MCAO agrees well with a neuroprotective role of BDNF in cortical neurons. However, elevated levels of NGF and BDNF protein could also increase synaptic efficacy in the postischemic phase, which may promote epileptogenesis.
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  • Lindberg, Bo G., et al. (författare)
  • Nubbin isoform antagonism governs Drosophila intestinal immune homeostasis
  • 2018
  • Ingår i: PLoS Pathogens. - : Public Library of Science (PLoS). - 1553-7366 .- 1553-7374. ; 14:3
  • Tidskriftsartikel (refereegranskat)abstract
    • Gut immunity is regulated by intricate and dynamic mechanisms to ensure homeostasis despite a constantly changing microbial environment. Several regulatory factors have been described to participate in feedback responses to prevent aberrant immune activity. Little is, however, known about how transcriptional programs are directly tuned to efficiently adapt host gut tissues to the current microbiome. Here we show that the POU/Oct gene nubbin (nub) encodes two transcription factor isoforms, Nub-PB and Nub-PD, which antagonistically regulate immune gene expression in Drosophila. Global transcriptional profiling of adult flies overexpressing Nub-PB in immunocompetent tissues revealed that this form is a strong transcriptional activator of a large set of immune genes. Further genetic analyses showed that Nub-PB is sufficient to drive expression both independently and in conjunction with nuclear factor kappa B (NF-κB), JNK and JAK/STAT pathways. Similar overexpression of Nub-PD did, conversely, repress expression of the same targets. Strikingly, isoform co-overexpression normalized immune gene transcription, suggesting antagonistic activities. RNAi-mediated knockdown of individual nub transcripts in enterocytes confirmed antagonistic regulation by the two isoforms and that both are necessary for normal immune gene transcription in the midgut. Furthermore, enterocyte-specific Nub-PB expression levels had a strong impact on gut bacterial load as well as host lifespan. Overexpression of Nub-PB enhanced bacterial clearance of ingested Erwinia carotovora carotovora 15. Nevertheless, flies quickly succumbed to the infection, suggesting a deleterious immune response. In line with this, prolonged overexpression promoted a proinflammatory signature in the gut with induction of JNK and JAK/STAT pathways, increased apoptosis and stem cell proliferation. These findings highlight a novel regulatory mechanism of host-microbe interactions mediated by antagonistic transcription factor isoforms.
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  • Lindvall, Johannes, 1975, et al. (författare)
  • Sweden: The Fall of the Strong State
  • 2006
  • Ingår i: SCANDINAVIAN POLITICAL STUDIES. - : Wiley. - 0080-6757 .- 1467-9477. ; 29:1, s. 47-63
  • Tidskriftsartikel (refereegranskat)abstract
    • From the 1930s to the 1980s, Swedish politics was based on the assumption that social change could be accomplished through a specific political and administrative process. National politicians decided the aims of policy, government commissions of inquiry engaged experts who compiled available knowledge, Parliament turned the resulting proposal into law, a civil service agency implemented the policy and local authorities put it into effect. This rationalistic model of social steering can be called 'the strong state'. This article documents the fall of the strong state. It also argues that these changes to the output side of government have troubling im-plications for the operation of democracy. The reason is that the strong state model provided citizens with a reasonably clear idea of how public policies were – or should be – produced and implemented. As a result of the strong state's decline, the link from elections to policy is partly obscure, partly broken. The question for the future is whether the strong state will be replaced by some new model that provides the necessary focal points for debates on public policy, or whether stable norms will remain absent due to an inherently obscure division of labour within Sweden's policy-making and administrative structures.
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  • Lindvall, Johannes, 1975, et al. (författare)
  • Vägar till välstånd
  • 2010
  • Bok (övrigt vetenskapligt/konstnärligt)
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18.
  • Lindvall, O., et al. (författare)
  • Differential regulation of mRNAs for nerve growth factor, brain-derived neurotrophic factor, and neurotrophin 3 in the adult rat brain following cerebral ischemia and hypoglycemic coma
  • 1992
  • Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 0027-8424. ; 89:2, s. 648-652
  • Tidskriftsartikel (refereegranskat)abstract
    • In situ hybridization was used to study expression of mRNAs for members of the nerve growth factor (NGF) family in the rat brain after 2 and 10 min of forebrain ischemia and 1 and 30 min of insulin-induced hypoglycemic coma. Two hours after the ischemic insults, the level of brain-derived neurotrophic factor (BDNF) mRNA was markedly increased in the granule cells of the dentate gyrus, and at 24 h it was still significantly elevated. NGF mRNA showed a pronounced increase 4 h after 2 min of ischemia but had returned to a control level at 24 h. Both 2 and 10 min of ischemia caused a clear reduction of the level of mRNA for neurotrophin 3 (NT-3) in the dentate granule cells and in regions CA2 and medial CA1 of the hippocampus 2 and 4 h after the insults. The increase of BDNF mRNA could be partially blocked by the α-amino-3- hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor antagonist NBQX but was not influenced by the N-methyl-D-aspartate (NMDA) receptor antagonist MK-801. Both NBQX and MK-801 attenuated the decrease of NT-3 mRNA after ischemia. One and 30 min of hypoglycemic coma also induced marked increases in BDNF and NGF mRNA in dentate granule cells with maximal levels at 2 h. If the changes of mRNA expression lead to alterations in the relative availability of neurotrophic factors, this could influence functional outcome and neuronal necrosis following ischemic and hypoglycemic insults.
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19.
  • Rothstein, Bo, 1954, et al. (författare)
  • The Fall of the Strong State
  • 2004
  • Ingår i: The Annual Meeting of the American Political Science Association.
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)
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20.
  • Svensson, Johanna, et al. (författare)
  • Societal Value of Stem Cell Therapy in Stroke - A Modeling Study.
  • 2012
  • Ingår i: Cerebrovascular Diseases. - : S. Karger AG. - 1421-9786 .- 1015-9770. ; 33:6, s. 532-539
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Stroke is one of the major causes of disability in the adult population and represents a heavy social and economic burden. Currently available therapeutic tools to support the recovery of impaired brain functions are quite limited. Animal studies have demonstrated that neuronal replacement and partial reconstruction of neural circuitry or modulation of the recovery process is possible with cell transplantation in the damaged adult brain. Stem cell therapy (SCT) may promote functional recovery also in stroke patients, thereby improving quality of life and reducing costs. Our aim was to estimate the potential societal value of SCT in stroke patients. Methods: We created a decision-analytic model in Microsoft Excel 2010 to assess life-long costs and quality-adjusted life years (QALYs) of SCT versus standard care for stroke patients from a societal perspective. The model structure consisted of 7 health states in accordance with the modified Rankin Scale (mRS). We modeled for age (55, 65, and 75 years), functional status at discharge (mRS 2, 3, and 4), effectiveness of SCT (50 and 25% increase in the probability to improve 1 mRS grade), mode of stem cell administration, risk of recurrent stroke, complications of intervention, and use of immunosuppressive drugs. The difference between an assumed societal willingness to pay for a QALY gain in Sweden (110,400 USD) and the cost per QALY gain resulting from the model was interpreted as the value of SCT. Results: Increased survival (1.06 life years) and improved functional status gave rise to an estimated gain of 1.34 QALY in a cohort of patients aged 55 with mRS 2 at hospital discharge. Although the SCT intervention increased costs by 64,014 USD (excluding cost of stem cells), the costs of intervention were offset mainly by decreased productivity losses. In total, the intervention saved 19,055 USD, i.e., at a price of 19,055 USD for stem cells, the SCT would be cost neutral. The societal value of SCT was 166,500 USD. Conclusions: The application of the health-economic model to Sweden shows that in younger stroke patients with moderate disability, the societal value of SCT given a zero price of stem cells is 166,500 USD. Although the transplantation itself is more costly, SCT offers potential for cost offset and cost savings in a long-term perspective by reducing the disability after stroke. The therapy appeared cost effective under a wide range of assumptions. Hence, further research and development in stem cells suitable for stroke therapy could potentially produce great value to society.
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