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Eriksson, Andreas C
Alternative names
Publications (10 of 24) Show all publications
Sjölund, J., Eriksson Jarliden, A., Andersson, M., Knutsson, H. & Nordström, H. (2014). Skull Segmentation in MRI by a Support Vector Machine Combining Local and Global Features. In: 22nd International Conference on Pattern Recognition (ICPR), 2014: . Paper presented at 22nd International Conference on Pattern Recognition (ICPR), 2014, 24-28 August, Stockholm, Sweden (pp. 3274-3279). IEEE
Open this publication in new window or tab >>Skull Segmentation in MRI by a Support Vector Machine Combining Local and Global Features
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2014 (English)In: 22nd International Conference on Pattern Recognition (ICPR), 2014, IEEE , 2014, p. 3274-3279Conference paper, Published paper (Refereed)
Abstract [en]

Magnetic resonance (MR) images lack information about radiation transport-a fact which is problematic in applications such as radiotherapy planning and attenuation correction in combined PET/MR imaging. To remedy this, a crude but common approach is to approximate all tissue properties as equivalent to those of water. We improve upon this using an algorithm that automatically identifies bone tissue in MR. More specifically, we focus on segmenting the skull prior to stereotactic neurosurgery, where it is common that only MR images are available. In the proposed approach, a machine learning algorithm known as a support vector machine is trained on patients for which both a CT and an MR scan are available. As input, a combination of local and global information is used. The latter is needed to distinguish between bone and air as this is not possible based only on the local image intensity. A whole skull segmentation is achievable in minutes. In a comparison with two other methods, one based on mathematical morphology and the other on deformable registration, the proposed method was found to yield consistently better segmentations.

Place, publisher, year, edition, pages
IEEE, 2014
Series
International Conference on Pattern Recognition, ISSN 1051-4651
Keywords
Bones; Computed tomography; Image segmentation; Magnetic resonance imaging; Positron emission tomography; Support vector machines; Training
National Category
Physical Sciences
Identifiers
urn:nbn:se:liu:diva-113296 (URN)10.1109/ICPR.2014.564 (DOI)000359818003068 ()
Conference
22nd International Conference on Pattern Recognition (ICPR), 2014, 24-28 August, Stockholm, Sweden
Available from: 2015-01-15 Created: 2015-01-15 Last updated: 2018-01-16Bibliographically approved
Ljungberg, L., Persson, K., Eriksson, A., Green, H. & Whiss, P. (2013). Effects of nicotine, its metabolites and tobacco extracts on human platelet function in vitro. Toxicology in Vitro, 27(2), 932-938
Open this publication in new window or tab >>Effects of nicotine, its metabolites and tobacco extracts on human platelet function in vitro
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2013 (English)In: Toxicology in Vitro, ISSN 0887-2333, E-ISSN 1879-3177, Vol. 27, no 2, p. 932-938Article in journal (Refereed) Published
Abstract [en]

Cigarette smoking is a leading cause of cardiovascular disease. The cardiovascular effects of smoking are probably multifactorial, including effects on platelets. Previous reports investigating the effects of nicotine and tobacco on platelet function are inconsistent.

The present study investigated in vitro effects of nicotine, its major metabolites, tobacco extracts and extract of tobacco-free snuff on human platelets.

None of the metabolites cotinine, cotinine-N-oxide, nicotine-1′-N-oxide or trans-3′-hydroxycotinine (0.1–10 μM) affected platelet aggregation or P-selectin expression. Nicotine (10 μM) weakly increased platelet aggregation, whereas trans-3′-hydroxycotinine (0.1 μM) and nicotine-1′-N-oxide (1–10 μM) weakly inhibited adhesion to fibrinogen. To elucidate the influence of other tobacco compounds, we investigated the impact of moist tobacco and smoke extracts on platelet function. Filtered extracts of oral snuff, cigarette smoke and tobacco free snuff inhibited platelet adhesion concentration-dependently. The inhibitory effects of tobacco extracts on platelet adhesion were independent of nicotine content and the nitric-oxide-pathway and not mediated through a platelet-nicotine-receptor.

Taken together, tobacco extracts inhibit platelet activation during short-term in vitro challenge. As only limited effects of nicotine and nicotine metabolites were seen, the tobacco-induced platelet inhibition are likely induced by other compounds present in tobacco and tobacco free snuff.

Place, publisher, year, edition, pages
Elsevier, 2013
Keywords
Cigarette smoke, Moist tobacco, Nicotine metabolite, Platelet adhesion, Platelet aggregation, Snuff
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-91549 (URN)10.1016/j.tiv.2013.01.004 (DOI)000316642800050 ()
Note

Funding Agencies|Swedish Research Council||Cardiovascular Inflammatory Research Centre (CIRC, Linkoping University, Sweden)||Halsofonden (Linkoping, Sweden)||County Council of Ostergotland (Linkoping, Sweden)||Eleanora Demeroutis Foundation for Cardiovascular Research (Linkoping, Sweden)||Medical Advisory Council (Swedish Match Northern Europe AB)||

Available from: 2013-04-26 Created: 2013-04-26 Last updated: 2017-12-06
Eriksson, A. C. & Whiss, P. A. (2013). Nanomolar concentrations of adrenaline induce platelet adhesion in vitro.. Platelets, 24(2), 129-135
Open this publication in new window or tab >>Nanomolar concentrations of adrenaline induce platelet adhesion in vitro.
2013 (English)In: Platelets, ISSN 0953-7104, E-ISSN 1369-1635, Vol. 24, no 2, p. 129-135Article in journal (Refereed) Published
Abstract [en]

Adrenaline is a platelet activator having a resting plasma concentration of <1 nmol/l that increases to a few nmol/l during stress. However, most in vitro assays only detect effects of adrenaline in micromolar concentrations. This makes it difficult to estimate the relevance of in vitro data for the in vivo situation. The aim of this study was to investigate experimental conditions in vitro that could detect platelet effects of adrenaline in nanomolar concentrations. Platelet adhesion to albumin and collagen was evaluated with a static platelet adhesion assay. Our results show that 10 nmol/l adrenaline induced platelet adhesion to albumin in platelet-rich plasma (PRP) prepared at 140 × g, while 100 nmol/l was necessary in order to increase adhesion of platelets prepared at 220 × g. The mean platelet volume was increased after preparation at 140 × g, suggesting that large reactive platelets contributed to the increased adrenaline sensitivity. At optimal Mg(2+)-concentration, adhesion to collagen was increased by 10 nmol/l adrenaline irrespective of centrifugal force applied during PRP preparation. More specifically, we defined two populations where adhesion to collagen was increased by 10 nmol/l adrenaline either upon centrifugation at 140 × g but not 220 × g or vice versa. In some experiments, platelet adhesion to collagen was induced by 3 nmol/l adrenaline, which corresponds to concentrations achieved during stress in vivo. In summary, the static adhesion assay is able to detect platelet activating effects of adrenaline very close to physiological concentrations. This is rare for in vitro assays and motivates further research about adrenergic signalling in platelets.

Place, publisher, year, edition, pages
Informa Healthcare, 2013
Keywords
Platelet activation, centrifugation, albumin, collagen, mean platelet volume, magnesium
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-89140 (URN)10.3109/09537104.2012.672780 (DOI)000314477400007 ()22471400 (PubMedID)
Available from: 2013-02-22 Created: 2013-02-22 Last updated: 2017-12-06
Hallbäck, I., Hägg, S., Eriksson, A. & Whiss, P. (2012). In vitro effects of serotonin and noradrenaline reuptake inhibitors on human platelet adhesion and coagulation. Pharmacological Reports, 64(4), 979-983
Open this publication in new window or tab >>In vitro effects of serotonin and noradrenaline reuptake inhibitors on human platelet adhesion and coagulation
2012 (English)In: Pharmacological Reports, ISSN 1734-1140, Vol. 64, no 4, p. 979-983Article in journal (Refereed) Published
Abstract [en]

Background: Although several studies show that there is an increased risk of bleeding events during antidepressant treatment with selective serotonin reuptake inhibitors (SSRIs), few studies show direct effects in vitro of SSRIs on hemostasis. less thanbrgreater than less thanbrgreater thanMethods: This study was undertaken to investigate the effects on platelet adhesion and plasma coagulation (APTT and PT) of two common SSRIs, citalopram and sertraline, the selective noradrenaline reuptake inhibitor reboxetine, and the serotonin and noradrenaline reuptake inhibitor venlafaxine. less thanbrgreater than less thanbrgreater thanResults: None of the compounds affected plasma coagulation significantly but all compounds except for venlafaxine inhibited platelet adhesion by approximately 50% or more at the highest concentration (100 mu g/l, p andlt; 0.01). The potency of respective compound to inhibit platelet adhesion to both collagen and fibrinogen surfaces was in the following order; citalopram andgt; sertraline andgt; reboxetine. In contrast, venlafaxine caused a weak but statistically significant increased platelet adhesion to fibrinogen. less thanbrgreater than less thanbrgreater thanConclusion: This study showed that sertraline, citalopram and reboxetine direct and acutely decrease platelet adhesion to both collagen and fibrinogen in vitro. These results also indicate that increased risk for bleeding complications in antidepressant users may not only be explained by depletion of serotonin in platelets.

Place, publisher, year, edition, pages
Inst. of Pharmacology, Polish Acad. of Sciences, 2012
Keywords
platelet activation, blood coagulation, SSRI, antidepressive agents, adverse effects
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-86662 (URN)10.1016/s1734-1140(12)70894-0 (DOI)000310420500022 ()
Note

Funding Agencies|Carl Gustav and Lilly Lennhoffs Foundation at the Swedish Academy of Pharmaceutical Sciences||

Available from: 2012-12-20 Created: 2012-12-20 Last updated: 2014-10-28Bibliographically approved
Eriksson, A., Lotfi, K. & Whiss, P. (2010). Correction: Enhanced platelet adhesion in essential thrombocythemia after in vitro activation (vol 27 pg 82, 2010). Turkish Journal of Hematology, 27(3), 223-223
Open this publication in new window or tab >>Correction: Enhanced platelet adhesion in essential thrombocythemia after in vitro activation (vol 27 pg 82, 2010)
2010 (English)In: Turkish Journal of Hematology, ISSN 1300-7777, E-ISSN 1308-5263, Vol. 27, no 3, p. 223-223Article in journal (Other academic) Published
Abstract [en]

n/a

Place, publisher, year, edition, pages
Aves Yayincilik, 2010
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-61173 (URN)000283186400018 ()
Available from: 2010-11-08 Created: 2010-11-05 Last updated: 2017-12-12Bibliographically approved
Eriksson, A. C., Lotfi, K. & Whiss, P. A. (2010). Enhanced platelet adhesion in essential thrombocythemia after in vitro activation. TURKISH JOURNAL OF HEMATOLOGY, 27(2), 82-90
Open this publication in new window or tab >>Enhanced platelet adhesion in essential thrombocythemia after in vitro activation
2010 (English)In: TURKISH JOURNAL OF HEMATOLOGY, ISSN 1300-7777, Vol. 27, no 2, p. 82-90Article in journal (Refereed) Published
Abstract [en]

Objective: Essential thrombocythemia (ET) is a chronic myeloproliferative disorder characterized by elevated platelet counts and increased risk of thrombosis. Ex vivo data suggest increased platelet reactivity in agreement with the increased thrombosis risk, while in vitro tests often detect decreased platelet activity. The present study aimed to investigate adhesion of ET-platelets in vitro, which is an aspect of platelet function that has been addressed in only a few studies on ET patients. Material and Methods: The study included 30 Er patients and 14 healthy controls. Platelet adhesion was measured with a static platelet adhesion assay. Results: The main finding was that ET-platelets were more readily activated by adhesion-inducing stimuli in vitro than control platelets. This was particularly evident in elderly patients and when using multiple stimuli, such as surfaces of collagen or fibrinogen combined with addition of adenosine 5-diphosphate or ristocetin. Such multiple stimuli resulted in adhesion above the control mean +2 standard deviations for approximately 50% of the patients. Conclusion: The results are in accordance with the concept of increased platelet activity in ET, but opposite to most other in vitro studies. We suggest that the conditions in the adhesion assay might mimic the in vivo situation regarding the presence of chronic platelet activation. (Turk J Hematol 2010; 27: 82-90)

Place, publisher, year, edition, pages
Aves Yayincilik, 2010
Keywords
Essential thrombocythemia; platelet activation; adhesion; thrombosis; platelet assay
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-13249 (URN)10.5152/tjh.2010.05 (DOI)000278947500005 ()
Available from: 2008-05-21 Created: 2008-05-21 Last updated: 2013-09-03
Felixsson, E., Persson, I.-L. A. L., Eriksson, A. C. & Persson, K. (2010). Horse chestnut extract contracts bovine vessels and affects human platelet aggregation through 5-HT(2A) receptors: an in vitro study. Phytotherapy Research, 24(9), 1297-1301
Open this publication in new window or tab >>Horse chestnut extract contracts bovine vessels and affects human platelet aggregation through 5-HT(2A) receptors: an in vitro study
2010 (English)In: Phytotherapy Research, ISSN 0951-418X, E-ISSN 1099-1573, Vol. 24, no 9, p. 1297-1301Article in journal (Refereed) Published
Abstract [en]

Extract from seeds and bark of horse chestnut (Aesculus hippocastanum L) is used as an herbal medicine against chronic venous insufficiency. The effect and mechanism of action on veins, arteries, and platelets are not fully understood. The aim of this study was to investigate the effects and mechanisms of action of horse chestnut on the contraction of bovine mesenteric veins and arteries, and human platelet aggregation. Contraction studies showed that horse chestnut extract dose-dependently contracted both veins and arteries, with the veins being the most sensitive. Contraction of both veins and arteries were significantly inhibited by the 5-HT(2A) receptor antagonist ketanserin. No effect on contraction was seen with the cyclooxygenase inhibitor indomethacin, the alpha(1) receptor antagonist prazosin or the angiotensin AT(1) receptor antagonist saralasin neither in veins nor arteries. ADP-induced human platelet aggregation was significantly reduced by horse chestnut. A further reduction was seen with the extract in the presence of ketanserin. In conclusion, horse chestnut contraction of both veins and arteries is, at least partly, mediated through 5-HT(2A) receptors. Human platelet aggregation is reduced by horse chestnut. The clinical importance of these findings concerning clinical use, possible adverse effects, and drug interactions remains to be investigated. Copyright (c) 2010 John Wiley & Sons, Ltd.

Keywords
arterial contraction; 5-HT; horse chestnut extract; platelet aggregation; venous contraction.
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-59047 (URN)10.1002/ptr.3103 (DOI)20148408 (PubMedID)
Available from: 2010-09-07 Created: 2010-09-07 Last updated: 2017-12-12Bibliographically approved
Fägerstam, P., Östberg, A. K., Eriksson, A., Fransson, S.-G. & Whiss, P. (2010). Similar inhibition of platelet adhesion, P-selectin expression and plasma coagulation by ioversol, iodixanol and ioxaglate. The British Journal of Radiology, 83(989), 401-410
Open this publication in new window or tab >>Similar inhibition of platelet adhesion, P-selectin expression and plasma coagulation by ioversol, iodixanol and ioxaglate
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2010 (English)In: The British Journal of Radiology, ISSN 0007-1285, Vol. 83, no 989, p. 401-410Article in journal (Refereed) Published
Abstract [en]

Contrast media (CM) are reported to possess both pro-thrombotic and anticoagulant properties. The mechanisms are not clearly understood and early reports are contradictory. To study the effects of CM on haemostasis, we analysed the ex vivo effects of ioversol and iodixanol on platelet adhesion and P-selectin expression, and the in vitro effects of ioversol, iodixanol and ioxaglate on platelet adhesion, P-selectin expression and plasma coagulation. A novel enzymatic assay was used to measure platelet adhesion to protein surfaces and an enzyme-linked immunosorbent assay was used to measure platelet P-selectin surface expression. Pro-thrombin time (PT) and activated partial thromboplastin time (APTT) were used to measure plasma coagulation. The ex vivo study consisted of blood from 27 outpatients administered ioversol and 9 patients administered iodixanol intravenously. Samples were collected before and 5 min after CM administration. Healthy donors were used for the in vitro studies on the effects of CM. The ex vivo study showed significantly (p<0.05) decreased platelet adhesion and P-selectin expression after administration of ioversol and iodixanol. Adhesion was more affected than P-selectin expression. The in vitro study showed that ioversol, iodixanol and ioaxaglate significantly (p<0.05) and dose dependently (beginning at 3 mg ml(-1)) decreased platelet adhesion and P-selectin expression. APTT and PT were significantly (p<0.01) prolonged at concentrations of 10 mg ml(-1) and 30 mg ml(-1), respectively. In conclusion, ioversol, iodixanol and ioxaglate inhibit platelet adhesion and P-selectin expression, as well as plasma coagulation. Platelets are more sensitive in relation to the inhibiting effect on plasma coagulation.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-20991 (URN)10.1259/bjr/71758045 (DOI)000277352900011 ()19546176 (PubMedID)
Available from: 2009-09-28 Created: 2009-09-28 Last updated: 2013-09-03
Eriksson, A. & Whiss , P. (2009). Characterization of static adhesion of human platelets in plasma to protein surfaces in microplates. BLOOD COAGULATION and FIBRINOLYSIS, 20(3), 197-206
Open this publication in new window or tab >>Characterization of static adhesion of human platelets in plasma to protein surfaces in microplates
2009 (English)In: BLOOD COAGULATION and FIBRINOLYSIS, ISSN 0957-5235 , Vol. 20, no 3, p. 197-206Article in journal (Refereed) Published
Abstract [en]

Platelet adhesion is a complex and important event for prevention of blood loss after vessel injury. This study investigated fundamental adhesive mechanisms occurring in an in-vitro assay developed for the measurement of static adhesion of human platelets in plasma. The aim was to gain methodological knowledge that could be used for interpretations of results from other studies using this specific assay. Involvement of adhesive receptors was investigated by the use of various antibodies as well as therapeutic drugs (abciximab, eptifibatide and tirofiban). Inhibitors of adenosine 5-diphosphate receptors (cangrelor, MRS2179) and of thromboxane A(2) signalling (BM-531) were used to estimate the role of autocrine activation. Adhesion to collagen was found to be mainly mediated by alpha(2)beta(1) and to some extent by alpha(IIb)beta(3) Adhesion to fibrinogen was mediated by alpha IIb beta 3. In addition, adenosine 5-diphosphate-induced adhesion to albumin was dependent on alpha(IIb)beta(3). Furthermore, experiments with cangrelor and BM-531 showed that the majority of the adhesive interactions tested were dependent on adenosine 5-diphosphate or thromboxane A(2). We conclude that the mechanisms of adhesion measured by the static platelet adhesion assay are in accordance with the current knowledge regarding platelet activation and adhesion. Despite its simplicity, we suggest that this adhesion assay could be used as a screening device for the study of the influence of various surfaces and soluble substances on platelet adhesion.

Keywords
adhesion receptor, antiplatelet agents, autocrine signalling, platelet adhesion, platelet assay
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-18037 (URN)10.1097/MBC.0b013e328327353d (DOI)
Note
This is a non-final version of an article published in final form: Andreas Eriksson and Per Whiss , Characterization of static adhesion of human platelets in plasma to protein surfaces in microplates, 2009, BLOOD COAGULATION and FIBRINOLYSIS, (20), 3, 197-206. http://dx.doi.org/10.1097/MBC.0b013e328327353d Copyright: Lippincott Williams and Wilkins; 1999 http://www.lww.com/ Available from: 2009-05-14 Created: 2009-05-04 Last updated: 2013-09-03Bibliographically approved
Eriksson, A. & Whiss, P. (2009). Platelet adhesion to proteins in microplates: from experimental research to clinical evaluation of platelet function. In: : . Paper presented at Congress of the International Society on Thrombosis and Haemostasis.
Open this publication in new window or tab >>Platelet adhesion to proteins in microplates: from experimental research to clinical evaluation of platelet function
2009 (English)Conference paper, Published paper (Refereed)
Abstract [en]

 Available platelet function assays differ with respect to the response they measure as well as in applicability, which range from experimental research to clinical evaluation of platelet function. This study focuses on the measurement of static adhesion of platelets in plasma to proteins in microplates. The aim was to describe fundamental adhesive events occurring in the assay and to investigate the ability to detect effects of factors acting both in vitro and in vivo. This communication combines several studies and presents novel interpretations. First of all, in vitro studies showed that platelets adhered to collagen via integrin alpha2beta1 whereas adhesion to surfaces coated with fibrinogen or albumin were dependent on alphaIIbbeta3. Elevated platelet adhesion, dependent on in vitro effects, was detected after addition of known platelet activators. The sensitivity of the assay is illustrated by significantly increased adhesion induced by 30 nmol/L epinephrine. Further in vitro studies showed that inhibition of autocrine activation decreased platelet adhesion. Also, adhesion was synergistically increased when combining two platelet activators at subthreshold levels. The detection of in vivo effects is illustrated by increased platelet adhesion for patients with the thrombosis prone disease essential thrombocythemia compared to healthy controls. The adhesion assay was reproducible in controls over time denoting that the assay can monitor platelet function. Decreased platelet adhesion was observed in vitro after addition of known platelet inhibitors and ex vivo after treatment with clopidogrel alone or in combination with acetylsalicylic acid in patients with a recent acute coronary syndrome. In conclusion, our studies show that this simple and flexible in vitro assay is able to detect elevated as well as decreased platelet adhesion both in vitro and ex vivo.

 

 

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-63262 (URN)
Conference
Congress of the International Society on Thrombosis and Haemostasis
Available from: 2010-12-14 Created: 2010-12-14 Last updated: 2014-06-23
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