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Hyötyläinen, T., Ghaffarzadegan, T., Karthikeyan, B. S., Triplett, E., Oresic, M. & Ludvigsson, J. (2024). Impact of Environmental Exposures on Human Breast Milk Lipidome in Future Immune-Mediated Diseases. Environmental Science and Technology, 58(5), 2214-2223
Open this publication in new window or tab >>Impact of Environmental Exposures on Human Breast Milk Lipidome in Future Immune-Mediated Diseases
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2024 (English)In: Environmental Science and Technology, ISSN 0013-936X, E-ISSN 1520-5851, Vol. 58, no 5, p. 2214-2223Article in journal (Refereed) Published
Abstract [en]

The composition of human breast milk (HBM) exhibits significant variability both between individuals and within the same individual. While environmental factors are believed to play a role in this variation, their influence on breast milk composition remains inadequately understood. Herein, we investigate the impact of environmental factors on HBM lipid composition in a general population cohort. The study included mothers (All Babies In Southeast Sweden study) whose children later progressed to one or more immune-mediated diseases later in life: type 1 diabetes (n = 9), celiac disease (n = 24), juvenile idiopathic arthritis (n = 9), inflammatory bowel disease (n = 7), hypothyroidism (n = 6), and matched controls (n = 173). Lipidome of HBM was characterized by liquid chromatography combined with high-resolution mass spectrometry. We observed that maternal age, body mass index, diet, and exposure to perfluorinated alkyl substances (PFASs) had a marked impact on breast milk lipidome, with larger changes observed in the milk of those mothers whose children later developed autoimmune diseases. We also observed differences in breast milk lipid composition in those mothers whose offspring later developed autoimmune diseases. Our study suggests that breast milk lipid composition is modified by a complex interaction between genetic and environmental factors, and, importantly, this impact was significantly more pronounced in those mothers whose offspring later developed autoimmune/inflammatory diseases. Our findings also suggest that merely assessing PFAS concentration may not capture the full extent of the impact of chemical exposures; thus, the more comprehensive exposome approach is essential for accurately assessing the impact of PFAS exposure on HBM and, consequently, on the health outcomes of the offspring.

Place, publisher, year, edition, pages
American Chemical Society (ACS), 2024
Keywords
Autoimmune diseases, human breast milk, lipidomics, maternal factors, perfluorinated alkyl substances
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:oru:diva-111048 (URN)10.1021/acs.est.3c06269 (DOI)001158427900001 ()38263945 (PubMedID)2-s2.0-85184299972 (Scopus ID)
Funder
Swedish Research Council, 2020-03674; 2016-05176; K2005-72X-11242-11A; K2008-69X-20826-01-4; K2008-69X-20826-01-4Swedish Research Council Formas, 2019-00869Novo Nordisk, NNF20OC0063971; NNF21OC0070309Swedish Child Diabetes FoundationForte, Swedish Research Council for Health, Working Life and Welfare, FAS2004-1775; FAS2004-1775Medical Research Council of Southeast Sweden (FORSS)Wallenberg Foundations, K 98-99D-12813-01Region ÖstergötlandLinköpings universitet
Note

This study was supported by the Swedish Research Council (grant nos. and 2020-03674 and 2016-05176 to T.H. and M.O.), Formas (grant no. 2019-00869 to T.H. and M.O.), and the Novo Nordisk Foundation (grant nos. NNF20OC0063971 and NNF21OC0070309 to T.H. and M.O.). ABIS study (J.L.) was supported by Barndiabetesfonden (Swedish Child Diabetes Foundation); the Swedish Council for Working Life and Social Research, grant/award numbers: FAS2004-1775 and FAS2004-1775; the Swedish Research Council, grant/award numbers: K2005-72X-11242-11A, K2008-69X-20826-01-4, and K2008-69X-20826-01-4; Östgöta Brandstodsbolag; the Medical Research Council of Southeast Sweden (FORSS); the Wallenberg Foundation, grant/award number: K 98-99D-12813-01A; ALF-and LFoU grants from Region Östergötland and Linköping university, Sweden; and Joanna Cocozza Foundation.

Available from: 2024-01-31 Created: 2024-01-31 Last updated: 2024-02-20Bibliographically approved
Hyötyläinen, T., McGlinchey, A. J., Salihovic, S., Schubert, A., Douglas, A., Hay, D. C., . . . Oresic, M. (2024). In utero exposures to perfluoroalkyl substances and the human fetal liver metabolome in Scotland: a cross-sectional study. The Lancet Planetary Health, 8(1), e5-e17
Open this publication in new window or tab >>In utero exposures to perfluoroalkyl substances and the human fetal liver metabolome in Scotland: a cross-sectional study
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2024 (English)In: The Lancet Planetary Health, E-ISSN 2542-5196, Vol. 8, no 1, p. e5-e17Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Perfluoroalkyl and polyfluoroalkyl substances are classed as endocrine disrupting compounds but continue to be used in many products such as firefighting foams, flame retardants, utensil coatings, and waterproofing of food packaging. Perfluoroalkyl exposure aberrantly modulates lipid, metabolite, and bile acid levels, increasing susceptibility to onset and severity of metabolic diseases, such as diabetes and metabolic dysfunction-associated steatotic liver disease. To date, most studies in humans have focused on perfluoroalkyl-exposure effects in adults. In this study we aimed to show if perfluoroalkyls are present in the human fetal liver and if they have metabolic consequences for the human fetus.

METHODS: In this cross-sectional study, human fetal livers from elective termination of pregnancies at the Aberdeen Pregnancy Counselling Service, Aberdeen, UK, were analysed by both targeted (bile acids and perfluoroalkyl substances) and combined targeted and untargeted (lipids and polar metabolites) mass spectrometry based metabolomic analyses, as well as with RNA-Seq. Only fetuses from normally progressing pregnancies (determined at ultrasound scan before termination), terminated for non-medical reasons, from women older than 16 years, fluent in English, and between 11 and 21 weeks of gestation were collected. Women exhibiting considerable emotional distress or whose fetuses had anomalies identified at ultrasound scan were excluded. Stringent bioinformatic and statistical methods such as partial correlation network analysis, linear regression, and pathway analysis were applied to this data to investigate the association of perfluoroalkyl exposure with hepatic metabolic pathways.

FINDINGS: Fetuses included in this study were collected between Dec 2, 2004, and Oct 27, 2014. 78 fetuses were included in the study: all 78 fetuses were included in the metabolomics analysis (40 female and 38 male) and 57 fetuses were included in the RNA-Seq analysis (28 female and 29 male). Metabolites associated with perfluoroalkyl were identified in the fetal liver and these varied with gestational age. Conjugated bile acids were markedly positively associated with fetal age. 23 amino acids, fatty acids, and sugar derivatives in fetal livers were inversely associated with perfluoroalkyl exposure, and the bile acid glycolithocholic acid was markedly positively associated with all quantified perfluoroalkyl. Furthermore, 7α-hydroxy-4-cholesten-3-one, a marker of bile acid synthesis rate, was strongly positively associated with perfluoroalkyl levels and was detectable as early as gestational week 12.

INTERPRETATION: Our study shows direct evidence for the in utero effects of perfluoroalkyl exposure on specific key hepatic products. Our results provide evidence that perfluoroalkyl exposure, with potential future consequences, manifests in the human fetus as early as the first trimester of gestation. Furthermore, the profiles of metabolic changes resemble those observed in perinatal perfluoroalkyl exposures. Such exposures are already linked with susceptibility, initiation, progression, and exacerbation of a wide range of metabolic diseases.

Place, publisher, year, edition, pages
Elsevier, 2024
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:oru:diva-110658 (URN)10.1016/S2542-5196(23)00257-7 (DOI)001158718400001 ()38199723 (PubMedID)2-s2.0-85181938990 (Scopus ID)
Funder
EU, Horizon EuropeEU, FP7, Seventh Framework ProgrammeSwedish Research CouncilSwedish Research Council FormasNovo Nordisk FoundationAcademy of Finland
Note

FUNDING: UK Medical Research Council, Horizon Europe Program of the European Union, Seventh Framework Programme of the European Union, NHS Grampian Endowments grants, European Partnership for the Assessment of Risks from Chemicals, Swedish Research Council, Formas, Novo Nordisk Foundation, and the Academy of Finland.

Available from: 2024-01-11 Created: 2024-01-11 Last updated: 2024-02-20Bibliographically approved
Laudette, M., Lindbom, M., Arif, M., Cinato, M., Ruiz, M., Doran, S., . . . Borén, J. (2023). Cardiomyocyte-specific PCSK9 deficiency compromises mitochondrial bioenergetics and heart function. Cardiovascular Research, 119(7), 1537-1552
Open this publication in new window or tab >>Cardiomyocyte-specific PCSK9 deficiency compromises mitochondrial bioenergetics and heart function
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2023 (English)In: Cardiovascular Research, ISSN 0008-6363, E-ISSN 1755-3245, Vol. 119, no 7, p. 1537-1552Article in journal (Refereed) Published
Abstract [en]

AIMS: PCSK9, which is expressed mainly in the liver and at low levels in the heart, regulates cholesterol levels by directing low-density lipoprotein receptors to degradation. Studies to determine the role of PCSK9 in the heart are complicated by the close link between cardiac function and systemic lipid metabolism. Here, we sought to elucidate the function of PCSK9 specifically in the heart by generating and analysing mice with cardiomyocyte-specific Pcsk9 deficiency (CM-Pcsk9-/- mice) and by silencing Pcsk9 acutely in a cell culture model of adult cardiomyocyte-like cells.

METHODS AND RESULTS: Mice with cardiomyocyte-specific deletion of Pcsk9 had reduced contractile capacity, impaired cardiac function and left ventricular dilatation at 28 weeks of age and died prematurely. Transcriptomic analyses revealed alterations of signalling pathways linked to cardiomyopathy and energy metabolism in hearts from CM-Pcsk9-/- mice versus wildtype littermates. In agreement, levels of genes and proteins involved in mitochondrial metabolism were reduced in CM-Pcsk9-/- hearts. By using a Seahorse flux analyser, we showed that mitochondrial but not glycolytic function was impaired in cardiomyocytes from CM-Pcsk9-/- mice. We further showed that assembly and activity of electron transport chain (ETC) complexes were altered in isolated mitochondria from CM-Pcsk9-/- mice. Circulating lipid levels were unchanged in CM-Pcsk9-/- mice, but the lipid composition of mitochondrial membranes was altered. In addition, cardiomyocytes from CM-Pcsk9-/- mice had an increased number of mitochondria-ER contacts and alterations in the morphology of cristae, the physical location of the ETC complexes. We also showed that acute Pcsk9 silencing in adult cardiomyocyte-like cells reduced the activity of ETC complexes and impaired mitochondrial metabolism.

CONCLUSION: PCSK9, despite its low expression in cardiomyocytes, contributes to cardiac metabolic function, and PCSK9 deficiency in cardiomyocytes is linked to cardiomyopathy, impaired heart function, and compromised energy production.

TRANSLATIONAL PERSPECTIVE: PCSK9 is mainly present in the circulation where it regulates plasma cholesterol levels. Here we show that PCSK9 mediates intracellular functions that differ from its extracellular functions. We further show that intracellular PCSK9 in cardiomyocytes, despite low expression levels, is important for maintaining physiological cardiac metabolism and function.

Place, publisher, year, edition, pages
Oxford University Press, 2023
Keywords
Pro-protein convertase subtilisin-kexin type 9 (PCSK9), cardiac dysfunction, cardiomyocyte, metabolic inflexibility, mitochondria
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:oru:diva-104809 (URN)10.1093/cvr/cvad041 (DOI)000950475500001 ()36880401 (PubMedID)2-s2.0-85165884933 (Scopus ID)
Funder
Swedish Research CouncilSwedish Heart Lung Foundation
Available from: 2023-03-08 Created: 2023-03-08 Last updated: 2023-12-08Bibliographically approved
Aye, C.-C., Hammond, D. E., Rodriguez-Cuenca, S., Doherty, M. K., Whitfield, P. D., Phelan, M. M., . . . Mora, S. (2023). CBL/CAP Is Essential for Mitochondria Respiration Complex I Assembly and Bioenergetics Efficiency in Muscle Cells. International Journal of Molecular Sciences, 24(4), Article ID 3399.
Open this publication in new window or tab >>CBL/CAP Is Essential for Mitochondria Respiration Complex I Assembly and Bioenergetics Efficiency in Muscle Cells
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2023 (English)In: International Journal of Molecular Sciences, ISSN 1661-6596, E-ISSN 1422-0067, Vol. 24, no 4, article id 3399Article in journal (Refereed) Published
Abstract [en]

CBL is rapidly phosphorylated upon insulin receptor activation. Mice whole body CBL depletion improved insulin sensitivity and glucose clearance; however, the precise mechanisms remain unknown. We depleted either CBL or its associated protein SORBS1/CAP independently in myocytes and assessed mitochondrial function and metabolism compared to control cells. CBL- and CAP-depleted cells showed increased mitochondrial mass with greater proton leak. Mitochondrial respiratory complex I activity and assembly into respirasomes were reduced. Proteome profiling revealed alterations in proteins involved in glycolysis and fatty acid degradation. Our findings demonstrate CBL/CAP pathway couples insulin signaling to efficient mitochondrial respiratory function and metabolism in muscle.

Place, publisher, year, edition, pages
MDPI, 2023
Keywords
CBL, SORBS1, glucose transport, insulin resistance, insulin signalling, mitochondria
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:oru:diva-104529 (URN)10.3390/ijms24043399 (DOI)000939225400001 ()36834818 (PubMedID)2-s2.0-85149028808 (Scopus ID)
Funder
European Commission
Note

Funding agencies:

University of Liverpool

European Commission Joint Research Centre HEALTH-F4-2008-223450

United States Department of Health & Human Services

National Institutes of Health (NIH) - USA GM105781

Instituto de Salud Carlos III-MINECO/European FEDER Funds PI17-00048

Scottish Funding Council and Highlands and Islands Enterprise

 

Available from: 2023-02-27 Created: 2023-02-27 Last updated: 2023-03-15Bibliographically approved
Lamichhane, S., Sen, P., Dickens, A. M., Kråkström, M., Ilonen, J., Lempainen, J., . . . Oresic, M. (2023). Circulating metabolic signatures of rapid and slow progression to type 1 diabetes in islet autoantibody-positive children. Frontiers in Endocrinology, 14, Article ID 1211015.
Open this publication in new window or tab >>Circulating metabolic signatures of rapid and slow progression to type 1 diabetes in islet autoantibody-positive children
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2023 (English)In: Frontiers in Endocrinology, E-ISSN 1664-2392, Vol. 14, article id 1211015Article in journal (Refereed) Published
Abstract [en]

AIMS/HYPOTHESIS: Appearance of multiple islet cell autoantibodies in early life is indicative of future progression to overt type 1 diabetes, however, at varying rates. Here, we aimed to study whether distinct metabolic patterns could be identified in rapid progressors (RP, disease manifestation within 18 months after the initial seroconversion to autoantibody positivity) vs. slow progressors (SP, disease manifestation at 60 months or later from the appearance of the first autoantibody).

METHODS: Longitudinal samples were collected from RP (n=25) and SP (n=41) groups at the ages of 3, 6, 12, 18, 24, or ≥ 36 months. We performed a comprehensive metabolomics study, analyzing both polar metabolites and lipids. The sample series included a total of 239 samples for lipidomics and 213 for polar metabolites.

RESULTS: We observed that metabolites mediated by gut microbiome, such as those involved in tryptophan metabolism, were the main discriminators between RP and SP. The study identified specific circulating molecules and pathways, including amino acid (threonine), sugar derivatives (hexose), and quinic acid that may define rapid vs. slow progression to type 1 diabetes. However, the circulating lipidome did not appear to play a major role in differentiating between RP and SP.

CONCLUSION/INTERPRETATION: Our study suggests that a distinct metabolic profile is linked with the type 1 diabetes progression. The identification of specific metabolites and pathways that differentiate RP from SP may have implications for early intervention strategies to delay the development of type 1 diabetes.

Place, publisher, year, edition, pages
Frontiers Media S.A., 2023
Keywords
Birth cohort, gut microbial metabolites, lipidomics, metabolomics, type 1 diabetes mellitus
National Category
Endocrinology and Diabetes
Identifiers
urn:nbn:se:oru:diva-108526 (URN)10.3389/fendo.2023.1211015 (DOI)001067529600001 ()37745723 (PubMedID)2-s2.0-85171890067 (Scopus ID)
Funder
Novo Nordisk Foundation, NNF18OC0034506Academy of Finland, 250114 323171 333981 337530
Note

This study was supported by the Novo Nordisk Foundation (NNF18OC0034506, to MO), Juvenile Diabetes Research Foundation (2-SRA-2014-159-Q-R, to MO, TH, RL, and MKn), Academy of Finland (Centre of Excellence in Molecular Systems Immunology and Physiology Research – SyMMyS, Decision No. 250114, to RL, JT, MO, RL, and MKn; and Personalised Health 2014 programme project, Decision No. 292568, to RL, JT, MO, RL, and MKn). Further support was received by the Academy of Finland postdoctoral grant (No. 323171 to SL) and (grant no. 333981 to MO), “Inflammation in human early life: targeting impacts on life-course health” (INITIALISE) consortium funded by the Horizon Europe Program of the European Union under Grant Agreement 101094099 (to MO), the Medical Research Funds, Tampere and Helsinki University Hospitals (to MKn), InFLAMES Flagship Programme of the Academy of Finland (decision number: 337530) and Turku University Hospital (to MO, RL, and JT).

Available from: 2023-09-25 Created: 2023-09-25 Last updated: 2024-01-31Bibliographically approved
Monfort-Pires, M., Lamichhane, S., Alonso, C., Egelandsdal, B., Oresic, M., Jordahl, V. O., . . . Haug, A. (2023). Classification of Common Food Lipid Sources Regarding Healthiness Using Advanced Lipidomics: A Four-Arm Crossover Study. International Journal of Molecular Sciences, 24(5), Article ID 4941.
Open this publication in new window or tab >>Classification of Common Food Lipid Sources Regarding Healthiness Using Advanced Lipidomics: A Four-Arm Crossover Study
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2023 (English)In: International Journal of Molecular Sciences, ISSN 1661-6596, E-ISSN 1422-0067, Vol. 24, no 5, article id 4941Article in journal (Refereed) Published
Abstract [en]

Prospective studies have failed to establish a causal relationship between animal fat intake and cardiovascular diseases in humans. Furthermore, the metabolic effects of different dietary sources remain unknown. In this four-arm crossover study, we investigated the impact of consuming cheese, beef, and pork meat on classic and new cardiovascular risk markers (obtained from lipidomics) in the context of a healthy diet. A total of 33 young healthy volunteers (23 women/10 men) were assigned to one out of four test diets in a Latin square design. Each test diet was consumed for 14 days, with a 2-week washout. Participants received a healthy diet plus Gouda- or Goutaler-type cheeses, pork, or beef meats. Before and after each diet, fasting blood samples were withdrawn. A reduction in total cholesterol and an increase in high density lipoprotein particle size were detected after all diets. Only the pork diet upregulated plasma unsaturated fatty acids and downregulated triglycerides species. Improvements in the lipoprotein profile and upregulation of circulating plasmalogen species were also observed after the pork diet. Our study suggests that, within the context of a healthy diet rich in micronutrients and fiber, the consumption of animal products, in particular pork meat, may not induce deleterious effects, and reducing the intake of animal products should not be regarded as a way of reducing cardiovascular risk in young individuals.

Place, publisher, year, edition, pages
MDPI, 2023
Keywords
Animal fat, beef meat, cardiovascular risk markers, cheese, lipidomics, liquid chromatography–mass spectrometry (LC-MS), pork meat
National Category
Nutrition and Dietetics Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:oru:diva-104896 (URN)10.3390/ijms24054941 (DOI)000948137900001 ()36902372 (PubMedID)2-s2.0-85149961786 (Scopus ID)
Note

Funding agency:

The Norwegian Agriculture Agency 281297

Available from: 2023-03-13 Created: 2023-03-13 Last updated: 2023-04-05Bibliographically approved
Hyötyläinen, T., Bagavathy Shanmugam, K., Ghaffarzadegan, T., Triplett, E. W., Oresic, M. & Ludvigsson, J. (2023). Cord serum metabolic signatures of future progression to immune-mediated diseases. iScience, 26(3), Article ID 106268.
Open this publication in new window or tab >>Cord serum metabolic signatures of future progression to immune-mediated diseases
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2023 (English)In: iScience, E-ISSN 2589-0042 , Vol. 26, no 3, article id 106268Article in journal (Refereed) Published
Abstract [en]

Previous prospective studies suggest that progression to autoimmune diseases is preceded by metabolic dysregulation, but it is not clear which metabolic changes are disease-specific and which are common across multiple immune-mediated diseases. Here we investigated metabolic profiles in cord serum in a general population cohort (All Babies In Southeast Sweden; ABIS), comprising infants who progressed to one or more immune-mediated diseases later in life: type 1 diabetes (n = 12), celiac disease (n = 28), juvenile idiopathic arthritis (n = 9), inflammatory bowel disease (n = 7), and hypothyroidism (n = 6); and matched controls (n = 270). We observed elevated levels of multiple triacylglycerols (TGs) an alteration in several gut microbiota related metabolites in the autoimmune groups. The most distinct differences were observed in those infants who later developed HT. The specific similarities observed in metabolic profiles across autoimmune diseases suggest that they share specific common metabolic phenotypes at birth that contrast with those of healthy controls.

Place, publisher, year, edition, pages
Cell Press, 2023
Keywords
Health sciences, Human metabolism, Immunology, Lipidomics, Metabolomics
National Category
Gastroenterology and Hepatology
Identifiers
urn:nbn:se:oru:diva-104968 (URN)10.1016/j.isci.2023.106268 (DOI)000995062700001 ()36915680 (PubMedID)2-s2.0-85150925263 (Scopus ID)
Funder
Swedish Research Council, 2020-03674 K2005-72 x -11242-11A K2008-69 x -20826-01-4Swedish Research Council Formas, 2019-00869Swedish Child Diabetes FoundationForte, Swedish Research Council for Health, Working Life and Welfare, FAS2004-1775Medical Research Council of Southeast Sweden (FORSS)Swedish Child Diabetes FoundationWallenberg Foundations, K 98-99D-12813-01ARegion ÖstergötlandLinköpings universitet
Note

Funding agency:

Östgöta Brandstodsbolag

Available from: 2023-03-15 Created: 2023-03-15 Last updated: 2023-06-13Bibliographically approved
Mathema, V. B., Sen, P., Lamichhane, S., Oresic, M. & Khoomrung, S. (2023). Deep learning facilitates multi-data type analysis and predictive biomarker discovery in cancer precision medicine. Computational and Structural Biotechnology Journal, 21, 1372-1382
Open this publication in new window or tab >>Deep learning facilitates multi-data type analysis and predictive biomarker discovery in cancer precision medicine
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2023 (English)In: Computational and Structural Biotechnology Journal, E-ISSN 2001-0370, Vol. 21, p. 1372-1382Article, review/survey (Refereed) Published
Abstract [en]

Cancer progression is linked to gene-environment interactions that alter cellular homeostasis. The use of biomarkers as early indicators of disease manifestation and progression can substantially improve diagnosis and treatment. Large omics datasets generated by high-throughput profiling technologies, such as microarrays, RNA sequencing, whole-genome shotgun sequencing, nuclear magnetic resonance, and mass spectrometry, have enabled data-driven biomarker discoveries. The identification of differentially expressed traits as molecular markers has traditionally relied on statistical techniques that are often limited to linear parametric modeling. The heterogeneity, epigenetic changes, and high degree of polymorphism observed in oncogenes demand biomarker-assisted personalized medication schemes. Deep learning (DL), a major subunit of machine learning (ML), has been increasingly utilized in recent years to investigate various diseases. The combination of ML/DL approaches for performance optimization across multi-omics datasets produces robust ensemble-learning prediction models, which are becoming useful in precision medicine. This review focuses on the recent development of ML/DL methods to provide integrative solutions in discovering cancer-related biomarkers, and their utilization in precision medicine.

Place, publisher, year, edition, pages
Elsevier, 2023
Keywords
Cancer, Deep learning, Oncogene, Precision medicine, Reinforcement learning, Systems medicine
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:oru:diva-104507 (URN)10.1016/j.csbj.2023.01.043 (DOI)000933992600001 ()36817954 (PubMedID)2-s2.0-85147607641 (Scopus ID)
Note

Funding agencies:

Chalermphrakiat Grant from the Faculty of Medicine, Siriraj Hospital

Mahidol University R016420001

NSRF B16F640099

Available from: 2023-02-24 Created: 2023-02-24 Last updated: 2023-03-15Bibliographically approved
Kråkström, M., Dickens, A. M., Alves, M. A., Forssten, S. D., Ouwehand, A. C., Hyötyläinen, T., . . . Lamichhane, S. (2023). Dynamics of the Lipidome in a Colon Simulator. Metabolites, 13(3), Article ID 355.
Open this publication in new window or tab >>Dynamics of the Lipidome in a Colon Simulator
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2023 (English)In: Metabolites, ISSN 2218-1989, E-ISSN 2218-1989, Vol. 13, no 3, article id 355Article in journal (Refereed) Published
Abstract [en]

Current evidence suggests that gut microbiome-derived lipids play a crucial role in the regulation of host lipid metabolism. However, not much is known about the dynamics of gut microbial lipids within the distinct gut biogeographic. Here we applied targeted and untargeted lipidomics to in vitro-derived feces. Simulated intestinal chyme was collected from in vitro gut vessels (V1-V4), representing proximal to distal parts of the colon after 24 and 48 h with/without polydextrose treatment. In total, 44 simulated chyme samples were collected from the in vitro colon simulator. Factor analysis showed that vessel and time had the strongest impact on the simulated intestinal chyme lipid profiles. We found that levels of phosphatidylcholines, sphingomyelins, triacylglycerols, and endocannabinoids were altered in at least one vessel (V1-V4) during simulation. We also found that concentrations of triacylglycerols, diacylglycerols, and endocannabinoids changed with time (24 vs. 48 h of simulation). Together, we found that the simulated intestinal chyme revealed a wide range of lipids that remained altered in different compartments of the human colon model over time.

Place, publisher, year, edition, pages
MDPI, 2023
Keywords
Gut microbiome, in vitro colon simulator, lipidomics, metabolomics
National Category
Bioinformatics (Computational Biology)
Identifiers
urn:nbn:se:oru:diva-105217 (URN)10.3390/metabo13030355 (DOI)000958186800001 ()36984795 (PubMedID)2-s2.0-85151516411 (Scopus ID)
Available from: 2023-03-30 Created: 2023-03-30 Last updated: 2023-04-17Bibliographically approved
Salihovic, S., Nyström, N., Mathisen, C.-W. B., Andersen, S., Olbjørn, C., Perminow, G., . . . Halfvarson, J. (2023). Identification and validation of a lipidomic signature as a novel diagnostic biomarker of paediatric Inflammatory Bowel Disease. Journal of Crohn's & Colitis, 17(Suppl. 1), I76-I77, Article ID DOP14.
Open this publication in new window or tab >>Identification and validation of a lipidomic signature as a novel diagnostic biomarker of paediatric Inflammatory Bowel Disease
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2023 (English)In: Journal of Crohn's & Colitis, ISSN 1873-9946, E-ISSN 1876-4479, Vol. 17, no Suppl. 1, p. I76-I77, article id DOP14Article in journal, Meeting abstract (Other academic) Published
Place, publisher, year, edition, pages
Oxford University Press, 2023
National Category
Gastroenterology and Hepatology
Identifiers
urn:nbn:se:oru:diva-107222 (URN)000960367600055 ()
Available from: 2023-07-31 Created: 2023-07-31 Last updated: 2023-07-31Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0002-2856-9165

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