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Li, Wei
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Publications (10 of 59) Show all publications
Yuan, X., Ward, L., Forssell, C., Siraj, N. & Li, W. (2018). Carotid Atheroma From Men Has Significantly Higher Levels of Inflammation and Iron Metabolism Enabled by Macrophages. Stroke, 49(2), 419-425
Open this publication in new window or tab >>Carotid Atheroma From Men Has Significantly Higher Levels of Inflammation and Iron Metabolism Enabled by Macrophages
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2018 (English)In: Stroke, ISSN 0039-2499, E-ISSN 1524-4628, Vol. 49, no 2, p. 419-425Article in journal (Refereed) Published
Abstract [en]

Background and Purpose-Men differ from women in the manifestation of atherosclerosis and iron metabolism. Intraplaque hemorrhage and hemoglobin (Hb) catabolism by macrophages are associated with atherosclerotic lesion instability. The study aims were to investigate sex differences in (1) lesion severity in relation to blood Hb, (2) iron homeostasis in human carotid plaques, and (3) macrophage polarization within atheroma. Methods-The carotid artery samples from 39 men and 23 women were immunostained with cell markers for macrophages, smooth muscle cells, ferritin, and TfR1 (transferrin receptor 1), which were further analyzed according to sex in relation to iron, Hb, and lipids in circulation. Additionally, samples of predefined regions from human carotid atherosclerotic lesions, including internal controls, were used for proteomic analysis by mass spectrometry. Results-Male patients, compared with women, had larger necrotic cores and more plaque rupture, which were associated with higher levels of Hb. Atheroma of male patients had significantly higher levels of Hb in circulation and CD68 macrophages, ferritin, and TfR1 in lesions. CD68 macrophages were significantly correlated with ferritin and TfR1. Plaques from male patients comparatively possessed higher levels of inflammatory macrophage subsets, CD86 (M1) and CD163 (M2), but lower levels of STF (serotransferrin) and HPX (hemopexin). Conclusions-Male patients with carotid atheroma had more advanced and ruptured lesions associated with significantly higher levels of inflammatory macrophage infiltration and high iron stores in the blood and in their plaques. These findings help to understand sex differences and iron metabolism in atherosclerosis and factors related to atheroma progression.

Place, publisher, year, edition, pages
LIPPINCOTT WILLIAMS & WILKINS, 2018
Keywords
atherosclerosis; ferritins; hemoglobins; hemopexin; macrophages; male
National Category
Neurology
Identifiers
urn:nbn:se:liu:diva-144876 (URN)10.1161/STROKEAHA.117.018724 (DOI)000422928000035 ()29284736 (PubMedID)
Note

Funding Agencies|Swedish Heart-Lung Foundation; Torsten and Ragnar Soderbergs Foundation; Stroke Foundation; Olle Engkvist Foundation; Swedish Gamla Tjanarinnor Foundation; Linkoping University; Linkoping University Hospital Research Fund

Available from: 2018-02-09 Created: 2018-02-09 Last updated: 2019-05-02
Ward, L., Olausson, P., Li, W. & Yuan, X. (2018). Proteomics and multivariate modelling reveal sex-specific alterations in distinct regions of human carotid atheroma. Biology of Sex Differences, 9, Article ID 54.
Open this publication in new window or tab >>Proteomics and multivariate modelling reveal sex-specific alterations in distinct regions of human carotid atheroma
2018 (English)In: Biology of Sex Differences, ISSN 2042-6410, Vol. 9, article id 54Article in journal (Refereed) Published
Abstract [en]

BackgroundAtherosclerotic lesions are comprised of distinct regions with different proteomic profiles. Men and women develop differences in lesion phenotype, with lesions from women generally being more stable and less prone to rupture. We aimed to investigate the differences in proteomic profiles between sexes, including distinct lesion regions, to identify altered proteins that contribute to these differences observed clinically.MethodsCarotid endarterectomy samples (ten men/ten women) were obtained, and intraplaque biopsies from three distinct regions (internal control, fatty streak and plaque) were analysed by tandem-mass spectrometry. Multivariate statistical modelling, using orthogonal partial least square-discriminant analysis, was used to discriminate the proteomes between men and women.ResultsMultivariate discriminant modelling revealed proteins from 16 functional groups that displayed sex-specific associations. Additional statistics revealed ten proteins that display region-specific alterations when comparing sexes, including proteins related to inflammatory response, response to reactive oxygen species, complement activation, transport and blood coagulation. Transport protein afamin and blood coagulation proteins antithrombin-III and coagulation factor XII were significantly increased in plaque region from women. Inflammatory response proteins lysozyme C and phospholipase A2 membrane-associated were significantly increased in plaque region from men. Limitations with this study are the small sample size, limited patient information and lack of complementary histology to control for cell type differences between sexes.ConclusionsThis pilot study, for the first time, utilises a multivariate proteomic approach to investigate sexual dimorphism in human atherosclerotic tissue, and provides an essential proteomic platform for further investigations to help understand sexual dimorphism and plaque vulnerability in atherosclerosis.

Place, publisher, year, edition, pages
BMC, 2018
Keywords
Afamin; Atherosclerosis; Lysozyme C; Mass spectrometry; Serine protease inhibitors; Vulnerability
National Category
Medical Genetics
Identifiers
urn:nbn:se:liu:diva-153822 (URN)10.1186/s13293-018-0217-3 (DOI)000454616000001 ()30594242 (PubMedID)
Note

Funding Agencies|Swedish Heart Lung Foundation; Torsten and Ragnar Soderbergs Foundation; Stroke Foundation; Olle Engkvist Foundation; Swedish Gamla Tjanarinnor Foundation; Linkoping University Hospital Research Fund

Available from: 2019-01-11 Created: 2019-01-11 Last updated: 2019-05-02
Liang, W., Ward, L., Karlsson, H., Ljunggren, S., Li, W., Lindahl, M. & Yuan, X. (2016). Distinctive proteomic profiles among different regions of human carotid plaques in men and women. Scientific Reports, 6(26231)
Open this publication in new window or tab >>Distinctive proteomic profiles among different regions of human carotid plaques in men and women
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2016 (English)In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 6, no 26231Article in journal (Refereed) Published
Abstract [en]

The heterogeneity of atherosclerotic tissue has limited comprehension in proteomic and metabolomic analyses. To elucidate the functional implications, and differences between genders, of atherosclerotic lesion formation we investigated protein profiles from different regions of human carotid atherosclerotic arteries; internal control, fatty streak, plaque shoulder, plaque centre, and fibrous cap. Proteomic analysis was performed using 2-DE with MALDI-TOF, with validation using nLC-MS/MS. Protein mapping of 2-DE identified 52 unique proteins, including 15 previously unmapped proteins, of which 41 proteins were confirmed by nLC-MS/MS analysis. Expression levels of 18 proteins were significantly altered in plaque regions compared to the internal control region. Nine proteins showed site-specific alterations, irrespective of gender, with clear associations to extracellular matrix remodelling. Five proteins display gender-specific alterations with 2-DE, with two alterations validated by nLC-MS/MS. Gender differences in ferritin light chain and transthyretin were validated using both techniques. Validation of immunohistochemistry confirmed significantly higher levels of ferritin in plaques from male patients. Proteomic analysis of different plaque regions has reduced the effects of plaque heterogeneity, and significant differences in protein expression are determined in specific regions and between genders. These proteomes have functional implications in plaque progression and are of importance in understanding gender differences in atherosclerosis.

Place, publisher, year, edition, pages
NATURE PUBLISHING GROUP, 2016
National Category
Biochemistry and Molecular Biology
Identifiers
urn:nbn:se:liu:diva-129495 (URN)10.1038/srep26231 (DOI)000376554600001 ()27198765 (PubMedID)
Note

Funding Agencies|Swedish Heart Lung Foundation; Linkoping University Hospital Research foundation; Swedish Institute; China Scholarship Council

Available from: 2016-06-20 Created: 2016-06-20 Last updated: 2019-04-17
Johansson, M. E., Zhang, X.-Y., Edfeldt, K., Lundberg, A. M., Levin, M. C., Boren, J., . . . Yan, Z.-Q. (2014). Innate immune receptor NOD2 promotes vascular inflammation and formation of lipid-rich necrotic cores in hypercholesterolemic mice. European Journal of Immunology, 44(10), 3081-3092
Open this publication in new window or tab >>Innate immune receptor NOD2 promotes vascular inflammation and formation of lipid-rich necrotic cores in hypercholesterolemic mice
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2014 (English)In: European Journal of Immunology, ISSN 0014-2980, E-ISSN 1521-4141, Vol. 44, no 10, p. 3081-3092Article in journal (Refereed) Published
Abstract [en]

Atherosclerosis is an inflammatory disease associated with the activation of innate immune TLRs and nucleotide-binding oligomerization domain-containing protein (NOD)like receptor pathways. However, the function of most innate immune receptors in atherosclerosis remains unclear. Here, we show that NOD2 is a crucial innate immune receptor influencing vascular inflammation and atherosclerosis severity. 10-week stimulation with muramyl dipeptide (MDP), the NOD2 cognate ligand, aggravated atherosclerosis, as indicated by the augmented lesion burden, increased vascular inflammation and enlarged lipid-rich necrotic cores in Ldlr(-/-) mice. Myeloid-specific ablation of NOD2, but not its downstream kinase, receptor-interacting serine/threonine-protein kinase 2, restrained the expansion of the lipid-rich necrotic core in Ldlr(-/-) chimeric mice. In vitro stimulation of macrophages with MDP enhanced the uptake of oxidized low-density lipoprotein and impaired cholesterol efflux in concordance with upregulation of scavenger receptor A1/2 and downregulation of ATP-binding cassette transporter A1. Ex vivo stimulation of human carotid plaques with MDP led to increased activation of inflammatory signaling pathways p38 MAPK and NF-kappa B-mediated release of proinflammatory cytokines. Altogether, this study suggests that NOD2 contributes to the expansion of the lipid-rich necrotic core and promotes vascular inflammation in atherosclerosis.

Place, publisher, year, edition, pages
Wiley-VCH Verlag, 2014
Keywords
Atherosclerosis; Inflammation; Innate immunity; Nucleotide-binding oligomerization domain-containing protein 2; Pattern recognition receptor
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-112483 (URN)10.1002/eji.201444755 (DOI)000343827600024 ()25042478 (PubMedID)
Note

Funding Agencies|Swedish Research Council; Swedish Heart-Lung Foundation; European Union projects (Immunath, AtheroRemo, AtheroFlux); O. E. och Edla Johanssons vetenskapliga stiftelse; KI foundation; KI Joint funding postdoc position; Swedish Society for Medical Research; Chinese Scholarship Council; Peking University Health Science Center; National Health and Medical Research Council of Australia

Available from: 2014-11-28 Created: 2014-11-28 Last updated: 2017-12-05
Szymanowski, A., Li, W., Lundberg, A., Evaldsson, C., Nilsson, L., Backteman, K., . . . Jonasson, L. (2014). Soluble Fas ligand is associated with natural killer cell dynamics in coronary artery disease. Atherosclerosis, 233(2), 616-622
Open this publication in new window or tab >>Soluble Fas ligand is associated with natural killer cell dynamics in coronary artery disease
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2014 (English)In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 233, no 2, p. 616-622Article in journal (Refereed) Published
Abstract [en]

Objective: Apoptosis of natural killer (NK) cells is increased in patients with coronary artery disease (CAD) and may explain why NK cell levels are altered in these patients. Soluble forms of Fas and Fas ligand (L) are considered as markers of apoptosis. Here, we investigated whether plasma levels of Fas and FasL were associated with NK cell apoptosis and NK cell levels in CAD patients. Methods: Fas and FasL in plasma were determined by ELISA in 2 cohorts of CAD patients; one longitudinal study measuring circulating NK cells and apoptotic NK cells by flow cytometry 1 day, 3 months and 12 months after a coronary event and one cross-sectional study measuring NK cell apoptosis ex vivo. Both studies included matched healthy controls. Fas and FasL were also determined in supernatants from NK cells undergoing cytokine-induced apoptosis in cell culture. Results: In the 12-month longitudinal study, plasma FasL increased by 15% (p less than 0.001) and NK cell levels by 31% (p less than 0.05) while plasma Fas did not change. Plasma FasL and NK cell levels were significantly related at 3 months and 12 months, r = 0.40, p less than 0.01. Furthermore, plasma FasL, but not plasma Fas, correlated with NK cell apoptosis ex vivo in CAD patients, r = 0.54, p less than 0.05. In vitro, cytokine-induced apoptosis of NK cells resulted in abundant release of FasL. Conclusion: In CAD patients, FasL in plasma is associated with both apoptotic susceptibility of NK cells and dynamic changes in circulating NK cells. NK cells are also themselves a potential source of soluble FasL. Our findings link NK cell status to a soluble marker with possible atheroprotective effects thereby supporting a beneficial role of NK cells in CAD.

Place, publisher, year, edition, pages
Elsevier, 2014
Keywords
Acute coronary syndrome; Coronary artery disease; Immune system; Leukocytes; Natural killer cells; Apoptosis
National Category
Cardiac and Cardiovascular Systems Cell and Molecular Biology
Identifiers
urn:nbn:se:liu:diva-106858 (URN)10.1016/j.atherosclerosis.2014.01.030 (DOI)000334337200045 ()
Available from: 2014-05-28 Created: 2014-05-23 Last updated: 2018-01-11
Miah, S., Zadeh, S. N., Yuan, X.-M. & Li, W. (2013). Expression of Egr1 and p53 in human carotid plaques and apoptosis induced by 7-oxysterol or p53.. Experimental and Toxicological Pathology, 65(5), 677-682
Open this publication in new window or tab >>Expression of Egr1 and p53 in human carotid plaques and apoptosis induced by 7-oxysterol or p53.
2013 (English)In: Experimental and Toxicological Pathology, ISSN 0940-2993, E-ISSN 1618-1433, Vol. 65, no 5, p. 677-682Article in journal (Refereed) Published
Abstract [en]

Egr-1 and p53 are involved in pathology of both atherosclerosis and cancer. However, it is unknown whether p53 and Egr1 are interactively involved in apoptosis in atherosclerosis. We found that in human carotid plaques, the expression of p53 was inversely correlated with Egr1. In U937 cells, 7 beta-hydroxycholesterol and 7-ketocholesterol induced production of reactive oxygen species (ROS), transient up-regulation of Egr1 followed by late induction of p53 and apoptosis. Cells with nuclear fragmentation induced by 7-oxysterol or p53 showed increased levels of p53, but decreased levels of Egr1. In conclusion, ROS induced by 7-oxysterols may function as an early initiator of Egr1 expression. The late induced p53 by 7-oxysterols contributes to apoptotic cell death and is linked to the reduction of Egr1 levels, which resembles the differential expression of p53 and Egr1 in human atheroma progression.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-90234 (URN)10.1016/j.etp.2012.08.002 (DOI)000322292700028 ()22999639 (PubMedID)
Available from: 2013-03-21 Created: 2013-03-21 Last updated: 2017-12-06
Laskar, A., Andersson, R. & Li, W. (2013). Fodipir and Its Dephosphorylated Derivative Dipyridoxyl Ethyldiamine Are Involved in Mangafodipir-Mediated Cytoprotection against 7 beta-Hydroxycholesterol-Induced Cell Death. Pharmacology, 92(3-4), 182-186
Open this publication in new window or tab >>Fodipir and Its Dephosphorylated Derivative Dipyridoxyl Ethyldiamine Are Involved in Mangafodipir-Mediated Cytoprotection against 7 beta-Hydroxycholesterol-Induced Cell Death
2013 (English)In: Pharmacology, ISSN 0031-7012, E-ISSN 1423-0313, Vol. 92, no 3-4, p. 182-186Article in journal (Refereed) Published
Abstract [en]

Objective: Mangafodipir exerts pharmacological effects, including vascular relaxation and protection against oxidative stress and cell death induced by oxysterols. Additionally, mangafodipir has been proposed for cardiovascular imaging. The primary metabolites of mangafodipir, manganese dipyridoxyl ethyldiamine (MnPLED) and its constituent dipyridoxyl diphosphate (Dp-dp) also known as fodipir, are pharmacologically active. However, whether they affect oxysterol-induced cytotoxicity is currently unknown. In this study, we examine whether the mangafodipir metabolite affects 7 beta-hydroxycholesterol (7 beta-OH)-induced cell death and identify the underlying mechanisms. Methods: U937 cells were pretreated or not with mangafodipir substrate (Ms; 200 pm), MnPLED (100 mu mol/l) or Dp-dp (100 mu mol/l) for 8 h and then exposed to 7 beta-OH (28 mu mol/l) for 18 h. Results: Our results revealed that pretreatment with MnPLED or Dp-dp protected against 7 beta-OH-induced cellular reactive oxygen species (ROS) production, apoptosis, and lysosomal membrane permeabilization (LMP). MnPLED and Dp-dp, in par with Ms, confer protection against 7 beta-OH-induced cytotoxicity by reducing cellular ROS and stabilization of the lysosomal membrane. Conclusion: These results suggest that fodipir is the pharmacologically active part in the structure of mangafodipir, which prevents 7 beta-OH-induced cell death by attenuating cellular ROS and by preventing LMP. In addition, MnPLED, which is the dephosphorylated product of fodipir, exerts a similar protective effect against 7 beta-OH-induced cytotoxicity. This result indicates that dephosphorylation of fodipir does not affect its pharmacological actions. Altogether our result confirms the cytoprotective effect of mangafodipir and justifies its potential use as a cytoprotective adjuvant.

Place, publisher, year, edition, pages
KARGER, ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND, 2013
Keywords
Atherosclerosis, Apoptosis, Mangafodipir, Oxidative stress, Oxysterols
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-102098 (URN)10.1159/000354601 (DOI)000326770700008 ()
Note

Funding Agencies|Swedish Heart Lung Foundation||Torsten and Ragnar Soderberg Foundation||Stroke Foundation||Olle Engkvist Foundation||Swedish Gamla Tjanarinnor Foundation||Linkoping University Linkoping University Hospital Research Foundation||Medical Research Council of Southeast Sweden||

Available from: 2013-11-29 Created: 2013-11-29 Last updated: 2017-12-06
Laskar, A., Andersson, R. G. & Li, W. (2013). Fodipir (Dp-dp) and its dephosphorylated derivative PLED are involved in mangafodipir mediated cyto-protection against 7β-hydroxycholesterol induced cell death.
Open this publication in new window or tab >>Fodipir (Dp-dp) and its dephosphorylated derivative PLED are involved in mangafodipir mediated cyto-protection against 7β-hydroxycholesterol induced cell death
2013 (English)Manuscript (preprint) (Other academic)
Abstract [en]

Mangafodipir exerts pharmacological effects, including vascular relaxation and protection against oxidative stress and cell death induced by oxysterols. Additionally, mangafodipir has been proposed for cardiovascular imaging. The primary metabolite of mangafodipir, manganese dipyridoxyl ethyldiamine (MnPLED) and its constituent, dipyridoxyl diphosphate (Dp-dp) also known as fodipir, are pharmacologically active. However, whether they affect oxysterol induced cytotoxicity is currently unknown. In this study, we examine whether the mangafodipir metabolite affects 7β-hydroxycholesterol (7βOH) induced cell death and identify the underlying mechanisms. U937 cells were pre-treated or not with mangafodipir substrate (Ms) (200 μm), MnPLED (100 μM) or Dp-dp (100 μM) for 8 hours and then exposed to 7βOH (28 μM) for 18 hours. Our results revealed that pre-treatment with MnPLED or Dp-dp protected against 7βOH induced cellular reactive oxygen species (ROS) production, apoptosis, and lysosomal membrane permeabilization (LMP). MnPLED and Dpdp in par with Ms, confer protection against 7βOH induced cytotoxicity by reducing  cellular ROS and stabilization of lysosomal membrane. These results suggest that, fodipir is the active part in mangafodipir, which shows the noted effects and its activity is conserved in MnPLED. These results further confirm the cyto-protective effect of mangafodipir and justify its potential use as a cyto-protective adjuvant.

Keywords
Atherogenic, Apoptosis, Mangafodipir, Oxidative stress, Oxysterols
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-91996 (URN)
Available from: 2013-05-07 Created: 2013-05-07 Last updated: 2013-05-07Bibliographically approved
Laskar, A., Eilertsen, J., Li, W. & Yuan, X.-M. (2013). SPION primes THP1 derived M2 macrophages towards M1-like macrophages. Biochemical and Biophysical Research Communications - BBRC, 441(4), 737-742
Open this publication in new window or tab >>SPION primes THP1 derived M2 macrophages towards M1-like macrophages
2013 (English)In: Biochemical and Biophysical Research Communications - BBRC, ISSN 0006-291X, E-ISSN 1090-2104, Vol. 441, no 4, p. 737-742Article in journal (Refereed) Published
Abstract [en]

Potentially, cellular iron regulates functional plasticity in macrophages yet; interaction of functionally polarized macrophages with iron-oxide nanoparticles has never been studied. We found that monocyte differentiation alters cellular ferritin and cathepsin L levels and induces functional polarization in macrophages. Iron in super paramagnetic iron-oxide nanoparticle (SPION) induces a phenotypic shift in THP1 derived M2 macrophages towards a high CD86+ macrophage subtype. This phenotypic shift was accompanied by up-regulated intracellular levels of ferritin and cathepsin L in M2 macrophages, which we found as a characteristic hallmark of M1 macrophages. Atherogenic oxysterols reduce phagocytic activity in both macrophage subtypes and thus these cells may escape detection by ironoxide nanoparticles (INPs) in-vivo.

Place, publisher, year, edition, pages
Elsevier, 2013
Keywords
Cathepsin L; Ferritin; Iron-oxide nanoparticles; M1 and M2 macrophages; Oxysterols
National Category
Immunology
Identifiers
urn:nbn:se:liu:diva-91999 (URN)10.1016/j.bbrc.2013.10.115 (DOI)000328434800008 ()
Available from: 2013-05-07 Created: 2013-05-07 Last updated: 2017-12-06Bibliographically approved
Li, W., Laskar, A., Sultana, N., Osman, E., Ghosh, M., Li, Q. & Yuan, X. (2012). Cell death induced by 7-oxysterols via lysosomal and mitochondrial pathways is p53-dependent. Free Radical Biology & Medicine, 53(11), 2054-2061
Open this publication in new window or tab >>Cell death induced by 7-oxysterols via lysosomal and mitochondrial pathways is p53-dependent
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2012 (English)In: Free Radical Biology & Medicine, ISSN 0891-5849, E-ISSN 1873-4596, Vol. 53, no 11, p. 2054-2061Article in journal (Refereed) Published
Abstract [en]

Oxysterol accumulation and p53 expression mainly in macrophages have been associated with cell death and necrotic core formation in human atheroma progression. Oxidative stress and lysosomal membrane permeabilization (LMP) in macrophages are important causes of macrophage apoptosis. However, it is not understood how p53 and oxysterols interact in the process. We show here that 7-oxysterols induce endogenous full-length p53 and phospho-p53 (p53-Ser15) in both nucleus and cytoplasm of THP1 and J774 cells, which is followed by cellular oxidative stress and apoptotic cell death. The role of p53 in 7-oxysterol-mediated cell death is further investigated in temperature sensitive p53-transfected (M1-t-p53) and in p53-deficient (M1) cells. These results reveal that 7-oxysterols induce induction and nuclear translocation of p53 in M1-t-p53 cells, which in turn enhances LMP, mitochondrial translocation of Bax, mitochondrial membrane permeabilization, cytosolic release of cytochrome c, and cell death. Most importantly, the above effects of 7-oxysterols were not observed in p53-deficient M1 cells. The findings reveal that 7-oxysterol-induced cell death occurs via p53-dependent pathways. Subsequent p53 nuclear translocation and induction of wild-type and phosphorylated p53 are early steps in oxysterol-induced lysosomal-mitochondrial pathways involved in cell death.

Place, publisher, year, edition, pages
Elsevier, 2012
Keywords
Apoptosis, Atherosclerosis, Bax, Lysosomes, Mitochondria, Oxidative stress, Free radicals
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-86892 (URN)10.1016/j.freeradbiomed.2012.09.007 (DOI)000312058300007 ()
Note

Funding Agencies|Swedish Heart Lung Foundation||Torsten and Ragnar Soderbergs Foundation||Stroke Foundation||Olle Engkvist Foundation||Swedish Gamla Tjanarinnor Foundation||Linkoping University||Linkoping University Hospital||

Available from: 2013-01-07 Created: 2013-01-07 Last updated: 2017-12-06
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