9 results on '"Sulek, Karolina"'
Search Results
2. Opportunities and barriers in omics-based biomarker discovery for steatotic liver diseases
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Hansen, Torben, Mann, Matthias, Matthijnssens, Jelle, Krag, Aleksander, Bork, Peer, Arumugam, Manimozhiyan, Trebicka, Jonel, Karsdal, Morten, Anastasiadou, Ema, Israelsen, Hans, Melberg, Hans Olav, Legido-Quigley, Cristina, Thiele, Maja, Villesen, Ida Falk, Niu, Lili, Johansen, Stine, Sulek, Karolina, Nishijima, Suguru, Espen, Lore Van, Keller, Marisa, Israelsen, Mads, Suvitaival, Tommi, Zawadzki, Andressa de, Juel, Helene Bæk, Brol, Maximilian Joseph, Stinson, Sara Elizabeth, Huang, Yun, Silva, Maria Camilla Alvarez, Kuhn, Michael, Leeming, Diana Julie, Dalgaard, Louise Torp, and Jensen, Lars Juhl
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- 2024
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3. OS-072-YI Identifying patterns of steatotic liver disease severity: a multiomic analysis of 834 distinct omics features from healthy to end-stage liver disease in 854 individuals
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Hansen, Johanne Kragh, primary, Nishijima, Suguru, additional, Schierwagen, Robert, additional, Holm, Louise Aas, additional, Sulek, Karolina, additional, Suvitaival, Tommi, additional, Pedersen, Julie Steen, additional, Israelsen, Mads, additional, Torp, Nikolaj, additional, Johansen, Stine, additional, Fonvig, Cilius, additional, Martínez, Marta Guindo, additional, Stinson, Sara, additional, Huang, Yun, additional, Jensen, Rasmus Tanderup, additional, Stankevic, Evelina, additional, Kuhn, Michael, additional, Keller, Marisa Isabell, additional, Van Espen, Lore, additional, Alvarez-Silva, Camila, additional, Villesen, Ida Falk, additional, Thorhauge, Katrine, additional, Andersen, Peter, additional, Lindvig, Katrine, additional, de Zawadzki, Andressa, additional, Brol, Maximilian Joseph, additional, Nielsen, Trine, additional, Brøns, Charlotte, additional, Juel, Helene Baek, additional, Niu, Lili, additional, Holm, Jens-Christian, additional, Bendtsen, Flemming, additional, Karsdal, Morten, additional, Mann, Matthias, additional, Matthijnssens, Jelle, additional, Legido-Quigly, Cristina, additional, Trebicka, Jonel, additional, Arumugam, Manimozhiyan, additional, Thiele, Maja, additional, Jensen, Lars Juhl, additional, Bork, Peer, additional, Hansen, Torben, additional, and Krag, Aleksander, additional
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- 2024
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4. Unbiased Proteomic Exploration Suggests Overexpression of Complement Cascade Proteins in Plasma from Patients with Psoriasis Compared with Healthy Individuals.
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Kromann, Bjørn, Niu, Lili, Møller, Line B. P., Sølberg, Julie, Sulek, Karolina, Gyldenløve, Mette, Dyring-Andersen, Beatrice, Skov, Lone, and Løvendorf, Marianne B.
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BLOOD proteins ,COMPLEMENT activation ,PERIOSTIN ,PROTEOMICS ,PSORIASIS - Abstract
Knowledge about the molecular mechanisms underlying the systemic inflammation observed in psoriasis remains incomplete. In this study, we applied mass spectrometry-based proteomics to compare the plasma protein levels between patients with psoriasis and healthy individuals, aiming to unveil potential systemically dysregulated proteins and pathways associated with the disease. Plasma samples from adult patients with moderate-to-severe psoriasis vulgaris (N = 59) and healthy age- and sex-matched individuals (N = 21) were analyzed using liquid chromatography–tandem mass spectrometry. Patients did not receive systemic anti-psoriatic treatment for four weeks before inclusion. A total of 776 protein groups were quantified. Of these, 691 were present in at least 60% of the samples, providing the basis for the downstream analysis. We identified 20 upregulated and 22 downregulated proteins in patients with psoriasis compared to controls (p < 0.05). Multiple proteins from the complement system were upregulated, including C2, C4b, C5, and C9, and pathway analysis revealed enrichment of proteins involved in complement activation and formation of the terminal complement complex. On the other end of the spectrum, periostin was the most downregulated protein in sera from patients with psoriasis. This comprehensive proteomic investigation revealed significantly elevated levels of complement cascade proteins in psoriatic plasma, which might contribute to increased systemic inflammation in patients with psoriasis. [ABSTRACT FROM AUTHOR]
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- 2024
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5. Circulating metabolomic markers in association with overall burden of microvascular complications in type 1 diabetes
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Rotbain Curovic, Viktor, primary, Sørland, Brede A, additional, Hansen, Tine W, additional, Jain, Siddhi Y, additional, Sulek, Karolina, additional, Mattila, Ismo Matias, additional, Frimodt-Moller, Marie, additional, Trost, Kajetan, additional, Legido-Quigley, Cristina, additional, Theilade, Simone, additional, Tofte, Nete, additional, Winther, Signe Abitz, additional, Hansen, Christian Stevns, additional, Rossing, Peter, additional, and Ahluwalia, Tarunveer S, additional
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- 2024
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6. Review: Opportunities and barriers for omics-based biomarker discovery in steatotic liver diseases
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Thiele, Maja, primary, Villesen, Ida Falk, additional, Niu, Lili, additional, Johansen, Stine, additional, Sulek, Karolina, additional, Nishijima, Suguru, additional, Van Espen, Lore, additional, Keller, Marisa, additional, Israelsen, Mads, additional, Suvitaival, Tommi, additional, de Zawadzki, Andressa, additional, Juel, Helene Bæk, additional, Brol, Maximilian Joseph, additional, Stinson, Sara Elisabeth, additional, Huang, Yun, additional, Alvarez Silva, Maria Camilla, additional, Kuhn, Michael, additional, Anastasiadou, Ema, additional, Leeming, Diana Julie, additional, Karsdal, Morten, additional, Matthijnssens, Jelle, additional, Arumugam, Manimozhiyan, additional, Dalgaard, Louise Torp, additional, Legido-Quigley, Cristina, additional, Mann, Mathias, additional, Trebicka, Jonel, additional, Bork, Peer, additional, Jensen, Lars Juhl, additional, Hansen, Torben, additional, Krag, Aleksander, additional, Israelsen, Hans, additional, Melberg, Hans Olav, additional, Thiele, Maja, additional, and Mann, Matthias, additional
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- 2024
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7. Circulating metabolomic markers in association with overall burden of microvascular complications in type 1 diabetes
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Rotbain Curovic, Viktor, Sørland, Brede A., Hansen, Tine W., Jain, Siddhi Y., Sulek, Karolina, Mattila, Ismo Matias, Frimodt-Moller, Marie, Trost, Kajetan, Legido-Quigley, Cristina, Theilade, Simone, Tofte, Nete, Winther, Signe Abitz, Hansen, Christian Stevns, Rossing, Peter, Ahluwalia, Tarunveer S., Rotbain Curovic, Viktor, Sørland, Brede A., Hansen, Tine W., Jain, Siddhi Y., Sulek, Karolina, Mattila, Ismo Matias, Frimodt-Moller, Marie, Trost, Kajetan, Legido-Quigley, Cristina, Theilade, Simone, Tofte, Nete, Winther, Signe Abitz, Hansen, Christian Stevns, Rossing, Peter, and Ahluwalia, Tarunveer S.
- Abstract
ntroduction Diabetic retinopathy (DR), diabetic kidney disease (DKD) and distal symmetric polyneuropathy (DSPN) share common pathophysiology and pose an additive risk of early mortality. Research design and methods In adults with type 1 diabetes, 49 metabolites previously associated with either DR or DKD were assessed in relation to presence of DSPN. Metabolites overlapping in significance with presence of all three complications were assessed in relation to microvascular burden severity (additive number of complications—ie, presence of DKD±DR±DSPN) using linear regression models. Subsequently, the same metabolites were assessed with progression to endpoints: soft microvascular events (progression in albuminuria grade, ≥30% estimated glomerular filtration rate (eGFR) decline, or any progression in DR grade), hard microvascular events (progression to proliferative DR, chronic kidney failure, or ≥40% eGFR decline), and hard microvascular or macrovascular events (hard microvascular events, cardiovascular events (myocardial infarction, stroke, or arterial interventions), or cardiovascular mortality), using Cox models. All models were adjusted for sex, baseline age, diabetes duration, systolic blood pressure, HbA1c, body mass index, total cholesterol, smoking, and statin treatment. Results The full cohort investigated consisted of 487 participants. Mean (SD) follow-up was 4.8 (2.9, 5.7) years. Baseline biothesiometry was available in 202 participants, comprising the cross-sectional cohort. Eight metabolites were significantly associated with presence of DR, DKD, and DSPN, and six with additive microvascular burden severity. In the full cohort longitudinal analysis, higher levels of 3,4-dihydroxybutanoic acid (DHBA), 2,4-DHBA, ribonic acid, glycine, and ribitol were associated with development of events in both crude and adjusted models. Adding 3,4-DHBA, ribonic acid, and glycine to a traditional risk factor model improved the discrimination of hard micr, INTRODUCTION: Diabetic retinopathy (DR), diabetic kidney disease (DKD) and distal symmetric polyneuropathy (DSPN) share common pathophysiology and pose an additive risk of early mortality. RESEARCH DESIGN AND METHODS: In adults with type 1 diabetes, 49 metabolites previously associated with either DR or DKD were assessed in relation to presence of DSPN. Metabolites overlapping in significance with presence of all three complications were assessed in relation to microvascular burden severity (additive number of complications-ie, presence of DKD±DR±DSPN) using linear regression models. Subsequently, the same metabolites were assessed with progression to endpoints: soft microvascular events (progression in albuminuria grade, ≥30% estimated glomerular filtration rate (eGFR) decline, or any progression in DR grade), hard microvascular events (progression to proliferative DR, chronic kidney failure, or ≥40% eGFR decline), and hard microvascular or macrovascular events (hard microvascular events, cardiovascular events (myocardial infarction, stroke, or arterial interventions), or cardiovascular mortality), using Cox models. All models were adjusted for sex, baseline age, diabetes duration, systolic blood pressure, HbA1c, body mass index, total cholesterol, smoking, and statin treatment. RESULTS: The full cohort investigated consisted of 487 participants. Mean (SD) follow-up was 4.8 (2.9, 5.7) years. Baseline biothesiometry was available in 202 participants, comprising the cross-sectional cohort. Eight metabolites were significantly associated with presence of DR, DKD, and DSPN, and six with additive microvascular burden severity. In the full cohort longitudinal analysis, higher levels of 3,4-dihydroxybutanoic acid (DHBA), 2,4-DHBA, ribonic acid, glycine, and ribitol were associated with development of events in both crude and adjusted models. Adding 3,4-DHBA, ribonic acid, and glycine to a traditional risk factor model improved the discrimination of hard microvascular e
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- 2024
8. Lipid profiling identifies modifiable signatures of cardiometabolic risk in children and adolescents with obesity
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Huang, Yun, Sulek, Karolina, Stinson, Sara E., Holm, Louise Aas, Kim, Min, Trost, Kajetan, Hooshmand, Kourosh, Lund, Morten Asp Vonsild, Fonvig, Cilius E., Juel, Helene Bæk, Nielsen, Trine, Ängquist, Lars, Rossing, Peter, Thiele, Maja, Krag, Aleksander, Holm, Jens-Christian, Legido-Quigley, Cristina, and Hansen, Torben
- Abstract
Pediatric obesity is a progressive, chronic disease that can lead to serious cardiometabolic complications. Here we investigated the peripheral lipidome in 958 children and adolescents with overweight or obesity and 373 with normal weight, in a cross-sectional study. We also implemented a family-based, personalized program to assess the effects of obesity management on 186 children and adolescents in a clinical setting. Using mass spectrometry-based lipidomics, we report an increase in ceramides, alongside a decrease in lysophospholipids and omega-3 fatty acids with obesity metabolism. Ceramides, phosphatidylethanolamines and phosphatidylinositols were associated with insulin resistance and cardiometabolic risk, whereas sphingomyelins showed inverse associations. Additionally, a panel of three lipids predicted hepatic steatosis as effectively as liver enzymes. Lipids partially mediated the association between obesity and cardiometabolic traits. The nonpharmacological management reduced levels of ceramides, phospholipids and triglycerides, indicating that lowering the degree of obesity could partially restore a healthy lipid profile in children and adolescents.
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- 2024
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9. Opportunities and barriers in omics-based biomarker discovery for steatotic liver diseases.
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Thiele, Maja, Villesen, Ida Falk, Niu, Lili, Johansen, Stine, Sulek, Karolina, Nishijima, Suguru, Espen, Lore Van, Keller, Marisa, Israelsen, Mads, Suvitaival, Tommi, Zawadzki, Andressa de, Juel, Helene Bæk, Brol, Maximilian Joseph, Stinson, Sara Elizabeth, Huang, Yun, Silva, Maria Camilla Alvarez, Kuhn, Michael, Anastasiadou, Ema, Leeming, Diana Julie, and Karsdal, Morten
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BIOMARKERS , *LIVER diseases , *ALCOHOL as fuel , *INDIVIDUALIZED medicine , *REGULATORY approval - Abstract
The rising prevalence of liver diseases related to obesity and excessive use of alcohol is fuelling an increasing demand for accurate biomarkers aimed at community screening, diagnosis of steatohepatitis and significant fibrosis, monitoring, prognostication and prediction of treatment efficacy. Breakthroughs in omics methodologies and the power of bioinformatics have created an excellent opportunity to apply technological advances to clinical needs, for instance in the development of precision biomarkers for personalised medicine. Via omics technologies, biological processes from the genes to circulating protein, as well as the microbiome – including bacteria, viruses and fungi, can be investigated on an axis. However, there are important barriers to omics-based biomarker discovery and validation, including the use of semi-quantitative measurements from untargeted platforms, which may exhibit high analytical, inter- and intra-individual variance. Standardising methods and the need to validate them across diverse populations presents a challenge, partly due to disease complexity and the dynamic nature of biomarker expression at different disease stages. Lack of validity causes lost opportunities when studies fail to provide the knowledge needed for regulatory approvals, all of which contributes to a delayed translation of these discoveries into clinical practice. While no omics-based biomarkers have matured to clinical implementation, the extent of data generated has enabled the hypothesis-free discovery of a plethora of candidate biomarkers that warrant further validation. To explore the many opportunities of omics technologies, hepatologists need detailed knowledge of commonalities and differences between the various omics layers, and both the barriers to and advantages of these approaches. [ABSTRACT FROM AUTHOR]
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- 2024
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