uu.seUppsala University Publications
Change search
Link to record
Permanent link

Direct link
BETA
Nowak, Christoph
Publications (10 of 13) Show all publications
Stenemo, M., Nowak, C., Byberg, L., Sundström, J., Giedraitis, V., Lind, L., . . . Ärnlöv, J. (2018). Circulating proteins as predictors of incident heart failure in the elderly. European Journal of Heart Failure, 20(1), 55-62
Open this publication in new window or tab >>Circulating proteins as predictors of incident heart failure in the elderly
Show others...
2018 (English)In: European Journal of Heart Failure, ISSN 1388-9842, E-ISSN 1879-0844, Vol. 20, no 1, p. 55-62Article in journal (Refereed) Published
Abstract [en]

Aims

To identify novel risk markers for incident heart failure using proteomic profiling of 80 proteins previously associated with cardiovascular pathology.

Methods and results

Proteomic profiling (proximity extension assay) was performed in two community‐based prospective cohorts of elderly individuals without heart failure at baseline: the Prospective Investigation of the Vasculature in Uppsala Seniors [PIVUS, n = 901, median age 70.2 (interquartile range 70.0–70.3) years, 80 events]; and the Uppsala Longitudinal Study of Adult Men [ULSAM, n = 685, median age 77.8 (interquartile range 76.9–78.1) years, 90 events]. Twenty‐nine proteins were associated with incident heart failure in the discovery cohort PIVUS after adjustment for age and sex, and correction for multiple testing. Eighteen associations replicated in ULSAM. In pooled analysis of both cohorts, higher levels of nine proteins were associated with incident heart failure after adjustment for established risk factors: growth differentiation factor 15 (GDF‐15), T‐cell immunoglobulin and mucin domain 1 (TIM‐1), tumour necrosis factor‐related apoptosis‐inducing ligand receptor 2 (TRAIL‐R2), spondin‐1 (SPON1), matrix metalloproteinase‐12 (MMP‐12), follistatin (FS), urokinase‐type plasminogen activator surface receptor (U‐PAR), osteoprotegerin (OPG), and suppression of tumorigenicity 2 (ST2). Of these, GDF‐15, U‐PAR, MMP‐12, TRAIL‐R2, SPON1 and FS were associated with worsened echocardiographic left ventricular systolic function at baseline, while only TIM‐1 was positively associated with worsened diastolic function (P < 0.02 for all).

Conclusion

Proteomic profiling identified several novel associations between proteins involved in apoptosis, inflammation, matrix remodelling, and fibrinolysis with incident heart failure in elderly individuals. Our results encourage additional studies investigating the underlying mechanisms and the clinical utility of our findings.

Keywords
Biomarkers, Epidemiology, Heart failure, Left ventricular dysfunction, Proteomics, Risk prediction
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:uu:diva-334416 (URN)10.1002/ejhf.980 (DOI)000423809700007 ()28967680 (PubMedID)
Funder
EU, Horizon 2020, 634869Swedish Research Council, 2012-2215; 2015-03477; 221-2013-1673Marianne and Marcus Wallenberg Foundation, 2012.0082Swedish Heart Lung Foundation, 20140422; 20150429; 20120169Knut and Alice Wallenberg Foundation, 2013.0126Göran Gustafsson Foundation for promotion of scientific research at Uppala University and Royal Institute of Technology, 1637
Note

Tove Fall och Johan Ärnlöv delar på sistaförfattarskapet.

Available from: 2017-11-23 Created: 2017-11-23 Last updated: 2019-04-09Bibliographically approved
Nowak, C., Hetty, S., Salihovic, S., Castillejo-Lopez, C., Ganna, A., Cook, N. L., . . . Ingelsson, E. (2018). Glucose challenge metabolomics implicates medium-chain acylcarnitines in insulin resistance. Scientific Reports, 8, Article ID 8691.
Open this publication in new window or tab >>Glucose challenge metabolomics implicates medium-chain acylcarnitines in insulin resistance
Show others...
2018 (English)In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 8, article id 8691Article in journal (Refereed) Published
Abstract [en]

Insulin resistance (IR) predisposes to type 2 diabetes and cardiovascular disease but its causes are incompletely understood. Metabolic challenges like the oral glucose tolerance test (OGTT) can reveal pathogenic mechanisms. We aimed to discover associations of IR with metabolite trajectories during OGTT. In 470 non-diabetic men (age 70.6 +/- 0.6 years), plasma samples obtained at 0, 30 and 120 minutes during an OGTT were analyzed by untargeted liquid chromatography-mass spectrometry metabolomics. IR was assessed with the hyperinsulinemic-euglycemic clamp method. We applied age-adjusted linear regression to identify metabolites whose concentration change was related to IR. Nine trajectories, including monounsaturated fatty acids, lysophosphatidylethanolamines and a bile acid, were significantly associated with IR, with the strongest associations observed for medium-chain acylcarnitines C10 and C12, and no associations with L-carnitine or C2-, C8-, C14- or C16-carnitine. Concentrations of C10-and C12-carnitine decreased during OGTT with a blunted decline in participants with worse insulin resistance. Associations persisted after adjustment for obesity, fasting insulin and fasting glucose. In mouse 3T3-L1 adipocytes exposed to different acylcarnitines, we observed blunted insulin-stimulated glucose uptake after treatment with C10-or C12-carnitine. In conclusion, our results identify medium-chain acylcarnitines as possible contributors to IR.

National Category
Endocrinology and Diabetes
Identifiers
urn:nbn:se:uu:diva-357687 (URN)10.1038/s41598-018-26701-0 (DOI)000434252600004 ()29875472 (PubMedID)
Funder
Knut and Alice Wallenberg Foundation, 2013.0126Swedish Research Council, 2015-03477
Note

Tove Fall and Erik Ingelsson contributed equally to this work.

Available from: 2018-08-23 Created: 2018-08-23 Last updated: 2018-08-23Bibliographically approved
Pereira, M. J., Skrtic, S., Katsogiannos, P., Abrahamsson, N., Kullberg, J., Nowak, C. & Eriksson, J. W. (2017). CDKN2C expression is low in type 2 diabetes and associated with reduced lipid storage capacity in subcutaneous adipose tissue and elevated free fatty acid levels. Paper presented at 53rd Annual Meeting of the European-Association-for-the-Study-of-Diabetes (EASD), SEP 11-15, 2017, Lisbon, PORTUGAL. Diabetologia, 60(S1), S272-S272, Article ID 598.
Open this publication in new window or tab >>CDKN2C expression is low in type 2 diabetes and associated with reduced lipid storage capacity in subcutaneous adipose tissue and elevated free fatty acid levels
Show others...
2017 (English)In: Diabetologia, ISSN 0012-186X, E-ISSN 1432-0428, Vol. 60, no S1, p. S272-S272, article id 598Article in journal, Meeting abstract (Other academic) Published
National Category
Endocrinology and Diabetes
Identifiers
urn:nbn:se:uu:diva-347293 (URN)000408315001375 ()
Conference
53rd Annual Meeting of the European-Association-for-the-Study-of-Diabetes (EASD), SEP 11-15, 2017, Lisbon, PORTUGAL
Available from: 2018-04-04 Created: 2018-04-04 Last updated: 2018-04-04Bibliographically approved
Censin, J. C., Nowak, C., Cooper, N., Bergsten, P., Todd, J. A. & Fall, T. (2017). Childhood adiposity and risk of type 1 diabetes: A Mendelian randomization study. PLoS Medicine, 14(8), Article ID e1002362.
Open this publication in new window or tab >>Childhood adiposity and risk of type 1 diabetes: A Mendelian randomization study
Show others...
2017 (English)In: PLoS Medicine, ISSN 1549-1277, E-ISSN 1549-1676, Vol. 14, no 8, article id e1002362Article in journal (Refereed) Published
Abstract [en]

Background The incidence of type 1 diabetes (T1D) is increasing globally. One hypothesis is that increasing childhood obesity rates may explain part of this increase, but, as T1D is rare, intervention studies are challenging to perform. The aim of this study was to assess this hypothesis with a Mendelian randomization approach that uses genetic variants as instrumental variables to test for causal associations. Methods and findings We created a genetic instrument of 23 single nucleotide polymorphisms (SNPs) associated with childhood adiposity in children aged 2-10 years. Summary-level association results for these 23 SNPs with childhood-onset (<17 years) T1D were extracted from a meta-analysis of genome-wide association study with 5,913 T1D cases and 8,828 reference samples. Using inverse-variance weighted Mendelian randomization analysis, we found support for an effect of childhood adiposity on T1D risk (odds ratio 1.32, 95% CI 1.06-1.64 per standard deviation score in body mass index [SDS-BMI]). A sensitivity analysis provided evidence of horizontal pleiotropy bias (p = 0.04) diluting the estimates towards the null. We therefore applied Egger regression and multivariable Mendelian randomization methods to control for this type of bias and found evidence in support of a role of childhood adiposity in T1D (odds ratio in Egger regression, 2.76, 95% CI 1.40-5.44). Limitations of our study include that underlying genes and their mechanisms for most of the genetic variants included in the score are not known. Mendelian randomization requires large sample sizes, and power was limited to provide precise estimates. This research has been conducted using data from the Early Growth Genetics (EGG) Consortium, the Genetic Investigation of Anthropometric Traits (GIANT) Consortium, the Tobacco and Genetics (TAG) Consortium, and the Social Science Genetic Association Consortium (SSGAC), as well as meta-analysis results from a T1D genome-wide association study. Conclusions This study provides genetic support for a link between childhood adiposity and T1D risk. Together with evidence from observational studies, our findings further emphasize the importance of measures to reduce the global epidemic of childhood obesity and encourage mechanistic studies.

Place, publisher, year, edition, pages
PUBLIC LIBRARY SCIENCE, 2017
National Category
Endocrinology and Diabetes
Identifiers
urn:nbn:se:uu:diva-335245 (URN)10.1371/journal.pmed.1002362 (DOI)000408766300001 ()28763444 (PubMedID)
Available from: 2017-12-04 Created: 2017-12-04 Last updated: 2017-12-04Bibliographically approved
Mubanga, M., Byberg, L., Nowak, C., Egenvall, A., Magnusson, P. K., Ingelsson, E. & Fall, T. (2017). Dog ownership and the risk of cardiovascular disease and death: a nationwide cohort study. Scientific Reports, 7(1), Article ID 15821.
Open this publication in new window or tab >>Dog ownership and the risk of cardiovascular disease and death: a nationwide cohort study
Show others...
2017 (English)In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 7, no 1, article id 15821Article in journal (Refereed) Published
Abstract [en]

Dogs may be beneficial in reducing cardiovascular risk in their owners by providing social support and motivation for physical activity. We aimed to investigate the association of dog ownership with incident cardiovascular disease (CVD) and death in a register-based prospective nation-wide cohort (n = 3,432,153) with up to 12 years of follow-up. Self-reported health and lifestyle habits were available for 34,202 participants in the Swedish Twin Register. Time-to-event analyses with time-updated covariates were used to calculate hazard ratios (HR) with 95% confidence intervals (CI). In single- and multiple-person households, dog ownership (13.1%) was associated with lower risk of death, HR 0.67 (95% CI, 0.65-0.69) and 0.89 (0.87-0.91), respectively; and CVD death, HR 0.64 (0.59-0.70), and 0.85 (0.81-0.90), respectively. In single-person households, dog ownership was inversely associated with cardiovascular outcomes (HR composite CVD 0.92, 95% CI, 0.89-0.94). Ownership of hunting breed dogs was associated with lowest risk of CVD. Further analysis in the Twin Register could not replicate the reduced risk of CVD or death but also gave no indication of confounding by disability, comorbidities or lifestyle factors. In conclusion, dog ownership appears to be associated with lower risk of CVD in single-person households and lower mortality in the general population.

National Category
Public Health, Global Health, Social Medicine and Epidemiology Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:uu:diva-334415 (URN)10.1038/s41598-017-16118-6 (DOI)000415658600066 ()29150678 (PubMedID)
Funder
Swedish Research Council Formas, 2013-1673
Available from: 2017-11-23 Created: 2017-11-23 Last updated: 2018-08-24Bibliographically approved
Agarwal, D., Nowak, C., Zhang, N. R., Pusztai, L. & Hatzis, C. (2017). Functional germline variants as potential co-oncogenes. NPJ BREAST CANCER, 3, Article ID 46.
Open this publication in new window or tab >>Functional germline variants as potential co-oncogenes
Show others...
2017 (English)In: NPJ BREAST CANCER, ISSN 2374-4677, Vol. 3, article id 46Article in journal (Refereed) Published
Abstract [en]

Germline variants that affect the expression or function of proteins contribute to phenotypic variation in humans and likely determine individual characteristics and susceptibility to diseases including cancer. A number of high penetrance germline variants that increase cancer risk have been identified and studied, but germline functional polymorphisms are not typically considered in the context of cancer biology, where the focus is primarily on somatic mutations. Yet, there is evidence from familial cancers indicating that specific cancer subtypes tend to arise in carriers of high-risk germline variants (e.g., triple negative breast cancers in mutated BRCA carriers), which suggests that pre-existing germline variants may determine which complementary somatic driver mutations are needed to drive tumorigenesis. Recent genome sequencing studies of large breast cancer cohorts reported only a handful of highly recurrent driver mutations, suggesting that different oncogenic events drive individual cancers. Here, we propose that germline polymorphisms can function as oncogenic modifiers, or co-oncogenes, and these determine what complementary subsequent somatic events are required for full malignant transformation. Therefore, we propose that germline aberrations should be considered together with somatic mutations to determine what genes drive cancer and how they may be targeted.

Place, publisher, year, edition, pages
NATURE PUBLISHING GROUP, 2017
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:uu:diva-345127 (URN)10.1038/s41523-017-0051-5 (DOI)000423610700001 ()29177190 (PubMedID)
Funder
The Breast Cancer FoundationWenner-Gren Foundations
Available from: 2018-03-08 Created: 2018-03-08 Last updated: 2018-03-08Bibliographically approved
Nowak, C. (2017). Insulin Resistance: Causes, biomarkers and consequences. (Doctoral dissertation). Uppsala: Acta Universitatis Upsaliensis
Open this publication in new window or tab >>Insulin Resistance: Causes, biomarkers and consequences
2017 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

The worldwide increasing number of persons affected by largely preventable diseases like diabetes demands better prevention and treatment. Insulin is required for effective utilisation of circulating nutrients. Impaired responsiveness to insulin (insulin resistance, IR) is a hallmark of type 2 diabetes and independently raises the risk of heart attack and stroke. The pathophysiology of IR is incompletely understood. High-throughput measurement of large numbers of circulating biomarkers may provide new insights beyond established risk factors.

The aims of this thesis were to (i) use proteomics, metabolomics and genomics methods in large community samples to identify biomarkers of IR; (ii) assess biomarkers for risk prediction and insights into aetiology and consequences of IR; and (iii) use Mendelian randomisation analysis to assess causality.

In Study I, analysis of 80 circulating proteins in 70-to-77-year-old Swedes identified cathepsin D as a biomarker for IR and highlighted a tentative causal effect of IR on raised plasma tissue plasminogen activator levels. In Study II, nontargeted fasting plasma metabolomics was used to discover 52 metabolites associated with glycaemic traits in non-diabetic 70-year-old men. Replication in independent samples of several thousand persons provided evidence for a causal effect of IR on reduced plasma oleic acid and palmitoleic acid levels. In Study III, nontargeted metabolomics in plasma samples obtained at three time points during an oral glucose challenge in 70-year-old men identified associations between a physiologic measure of IR and concentration changes in medium-chain acylcarnitines, monounsaturated fatty acids, bile acids and lysophosphatidylethanolamines. Study IV provided evidence in two large longitudinal cohorts for causal effects of type 2 diabetes and impaired insulin secretion on raised coronary artery disease risk.

In conclusion, the Studies in this thesis provide new insights into the pathophysiology and adverse health consequences of IR and illustrate the value of combining traditional epidemiologic designs with recent molecular techniques and bioinformatics methods. The results provide limited evidence for the role of circulating proteins and small molecules in IR and require replication in separate studies and validation in experimental designs.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2017. p. 54
Series
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 1316
Keywords
insulin resistance, diabetes, insulin secretion, cardiovascular, mendelian randomization, proteomics, metabolomics, genomics, molecular epidemiology, complex disease, risk prediction, coronary heart disease, stroke, hyperglycemia
National Category
Basic Medicine Clinical Medicine Cell and Molecular Biology Endocrinology and Diabetes Public Health, Global Health, Social Medicine and Epidemiology Physiology
Identifiers
urn:nbn:se:uu:diva-316891 (URN)978-91-554-9856-6 (ISBN)
Public defence
2017-05-22, Room E10:1309 (BMC Navet), Biomedicinskt Centrum (BMC), Husargatan 3, Uppsala, 09:15 (English)
Opponent
Supervisors
Available from: 2017-04-28 Created: 2017-03-14 Last updated: 2018-01-13
Nowak, C., Salihovic, S., Ganna, A., Brandmaier, S., Tukiainen, T., Broeckling, C. D., . . . Fall, T. (2016). Effect of Insulin Resistance on Monounsaturated Fatty Acid Levels: A Multi-cohort Non-targeted Metabolomics and Mendelian Randomization Study. PLoS Genetics, 12(10), Article ID e1006379.
Open this publication in new window or tab >>Effect of Insulin Resistance on Monounsaturated Fatty Acid Levels: A Multi-cohort Non-targeted Metabolomics and Mendelian Randomization Study
Show others...
2016 (English)In: PLoS Genetics, ISSN 1553-7390, E-ISSN 1553-7404, Vol. 12, no 10, article id e1006379Article in journal (Refereed) Published
Abstract [en]

Insulin resistance (IR) and impaired insulin secretion contribute to type 2 diabetes and cardiovascular disease. Both are associated with changes in the circulating metabolome, but causal directions have been difficult to disentangle. We combined untargeted plasma metabolomics by liquid chromatography/mass spectrometry in three non-diabetic cohorts with Mendelian Randomization (MR) analysis to obtain new insights into early metabolic alterations in IR and impaired insulin secretion. In up to 910 elderly men we found associations of 52 metabolites with hyperinsulinemic-euglycemic clamp-measured IR and/or beta-cell responsiveness (disposition index) during an oral glucose tolerance test. These implicated bile acid, glycerophospholipid and caffeine metabolism for IR and fatty acid biosynthesis for impaired insulin secretion. In MR analysis in two separate cohorts (n = 2,613) followed by replication in three independent studies profiled on different metabolomics platforms (n = 7,824 / 8,961 / 8,330), we discovered and replicated causal effects of IR on lower levels of palmitoleic acid and oleic acid. A trend for a causal effect of IR on higher levels of tyrosine reached significance only in meta-analysis. In one of the largest studies combining "gold standard" measures for insulin responsiveness with non-targeted metabolomics, we found distinct metabolic profiles related to IR or impaired insulin secretion. We speculate that the causal effects on monounsaturated fatty acid levels could explain parts of the raised cardiovascular disease risk in IR that is independent of diabetes development.

National Category
Medical Genetics
Identifiers
urn:nbn:se:uu:diva-310027 (URN)10.1371/journal.pgen.1006379 (DOI)000386683300041 ()27768686 (PubMedID)
Funder
Knut and Alice Wallenberg Foundation, 2015.0327Swedish Diabetes Association, DIA 2013-024Göran Gustafsson Foundation for promotion of scientific research at Uppala University and Royal Institute of TechnologySwedish Heart Lung Foundation, 20120197 20150429 20070481EU, European Research Council, 33595 HEALTH-2009-2.2.1-3/242114 HEALTH-2013-2.4.2-1/602936Swedish Research Council, 2012-1397 2015-03477 M-2005-1112 2016-00250The Karolinska Institutet's Research FoundationNIH (National Institute of Health), DK U01-066134Swedish Foundation for Strategic Research
Available from: 2016-12-12 Created: 2016-12-09 Last updated: 2018-01-13Bibliographically approved
Nowak, C., Sundström, J., Gustafsson, S., Giedraitis, V., Lind, L., Ingelsson, E. & Fall, T. (2016). Protein Biomarkers for Insulin Resistance and Type 2 Diabetes Risk in Two Large Community Cohorts. Diabetes, 65(1), 276-284
Open this publication in new window or tab >>Protein Biomarkers for Insulin Resistance and Type 2 Diabetes Risk in Two Large Community Cohorts
Show others...
2016 (English)In: Diabetes, ISSN 0012-1797, E-ISSN 1939-327X, Vol. 65, no 1, p. 276-284Article in journal (Refereed) Published
Abstract [en]

Insulin resistance (IR) is a precursor of type 2 diabetes (T2D), and improved risk prediction and understanding of the pathogenesis are needed. We used a novel high-throughput 92-protein assay to identify circulating biomarkers for HOMA of IR in two cohorts of community residents without diabetes (n = 1,367) (mean age 73 ± 3.6 years). Adjusted linear regression identified cathepsin D and confirmed six proteins (leptin, renin, interleukin-1 receptor antagonist [IL-1ra], hepatocyte growth factor, fatty acid-binding protein 4, and tissue plasminogen activator [t-PA]) as IR biomarkers. Mendelian randomization analysis indicated a positive causal effect of IR on t-PA concentrations. Two biomarkers, IL-1ra (hazard ratio [HR] 1.28, 95% CI 1.03-1.59) and t-PA (HR 1.30, 1.02-1.65) were associated with incident T2D, and t-PA predicted 5-year transition to hyperglycemia (odds ratio 1.30, 95% CI 1.02-1.65). Additional adjustment for fasting glucose rendered both coefficients insignificant and revealed an association between renin and T2D (HR 0.79, 0.62-0.99). LASSO regression suggested a risk model including IL-1ra, t-PA, and the Framingham Offspring Study T2D score, but prediction improvement was nonsignificant (difference in C-index 0.02, 95% CI -0.08 to 0.12) over the T2D score only. In conclusion, proteomic blood profiling indicated cathepsin D as a new IR biomarker and suggested a causal effect of IR on t-PA.

National Category
Endocrinology and Diabetes
Identifiers
urn:nbn:se:uu:diva-270825 (URN)10.2337/db15-0881 (DOI)000367424900029 ()26420861 (PubMedID)
Funder
Swedish Research Council, 2012-1397Swedish Heart Lung Foundation, 20140422Swedish Diabetes Association, 2013-024Knut and Alice Wallenberg FoundationEU, European Research Council
Available from: 2016-01-04 Created: 2016-01-04 Last updated: 2017-12-01Bibliographically approved
Nowak, J., Nowak, C. & Odenbach, S. (2015). Consequences of Sheep Blood Used as Diluting Agent for the Magnetoviscous Effect in Biocompatible Ferrofluids. Applied Rheology, 25(5), 20-27, Article ID 53250.
Open this publication in new window or tab >>Consequences of Sheep Blood Used as Diluting Agent for the Magnetoviscous Effect in Biocompatible Ferrofluids
2015 (English)In: Applied Rheology, ISSN 1430-6395, E-ISSN 1617-8106, Vol. 25, no 5, p. 20-27, article id 53250Article in journal (Refereed) Published
Abstract [en]

Magnetic nanoparticles suspended in suitable carrier liquids can be adopted for use in biomedicine. For this to be achieved, the biocompatibility of these ferrofluids needs to be ascertained. In cancer treatment, potential applications currently under investigation include, e.g. drug targeting by using magneticfields and the destruction of diseased cells by applying alternating magnetic fields, which cause heating of magnetic nanoparticles. To enable the use of ferrofluids in the actual biomedical context, detailed knowledge of the flow characteristics is essential to ensure safe treatment. From ferrofluids used in the engineering context, a rise of viscosity when a magnetic field is applied the magnetoviscous effect is well known. This effect, which leads to an increased viscosity and profound alteration of a fluid's rheological behavior, has also been demonstrated for biocompatible ferrofluids used in the aforementioned applications. In biomedical applications, ferrofluids will be diluted in the blood stream. Therefore, the interaction between whole blood and the ferrofluid has to be investigated. This is the focus of the current experimental study, which makes use of two different ferrofluids diluted in sheep blood to gain a deeper understanding of the fluid mixtures primarily regarding the relative change in viscosity if an external magnetic field is applied. The results demonstrate a strong interaction between blood cells and structures formed by the magnetic nanoparticles and show a high deviation of results compared to ferrofluids diluted in water. These findings have to be taken into account for future research and applications of similar biocompatible fluids to guarantee safe and effective use in living organisms.

Keywords
Magnetoviscous effect, ferrofluid, rotational rheometry, magnetic nanoparticles, biomedical materials
National Category
Mechanical Engineering
Identifiers
urn:nbn:se:uu:diva-274717 (URN)10.3933/APPLRHEOL-25-53250 (DOI)000367278700008 ()
Available from: 2016-02-01 Created: 2016-01-25 Last updated: 2017-11-30Bibliographically approved
Organisations

Search in DiVA

Show all publications