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2. Genomic analysis of intracranial and subcortical brain volumes yields polygenic scores accounting for variation across ancestries

Author

García-Marín, Luis M., Campos, Adrian I., Diaz-Torres, Santiago, Rabinowitz, Jill A., Ceja, Zuriel, Mitchell, Brittany L., Grasby, Katrina L., Thorp, Jackson G., Agartz, Ingrid, Alhusaini, Saud, Ames, David, Amouyel, Philippe, Andreassen, Ole A., Arfanakis, Konstantinos, Arias-Vasquez, Alejandro, Armstrong, Nicola J., Athanasiu, Lavinia, Bastin, Mark E., Beiser, Alexa S., Bennett, David A., Bis, Joshua C., Boks, Marco P. M., Boomsma, Dorret I., Brodaty, Henry, Brouwer, Rachel M., Buitelaar, Jan K., Burkhardt, Ralph, Cahn, Wiepke, Calhoun, Vince D., Carmichael, Owen T., Chakravarty, Mallar, Chen, Qiang, Ching, Christopher R. K., Cichon, Sven, Crespo-Facorro, Benedicto, Crivello, Fabrice, Dale, Anders M., Smith, George Davey, de Geus, Eco J. C., De Jager, Philip L., de Zubicaray, Greig I., Debette, Stéphanie, DeCarli, Charles, Depondt, Chantal, Desrivières, Sylvane, Djurovic, Srdjan, Ehrlich, Stefan, Erk, Susanne, Espeseth, Thomas, Fernández, Guillén, Filippi, Irina, Fisher, Simon E., Fleischman, Debra A., Fletcher, Evan, Fornage, Myriam, Forstner, Andreas J., Francks, Clyde, Franke, Barbara, Ge, Tian, Goldman, Aaron L., Grabe, Hans J., Green, Robert C., Grimm, Oliver, Groenewold, Nynke A., Gruber, Oliver, Gudnason, Vilmundur, Håberg, Asta K., Haukvik, Unn K., Heinz, Andreas, Hibar, Derrek P., Hilal, Saima, Himali, Jayandra J., Ho, Beng-Choon, Hoehn, David F., Hoekstra, Pieter J., Hofer, Edith, Hoffmann, Wolfgang, Holmes, Avram J., Homuth, Georg, Hosten, Norbert, Ikram, M. Kamran, Ipser, Jonathan C., Jack Jr, Clifford R., Jahanshad, Neda, Jönsson, Erik G., Kahn, Rene S., Kanai, Ryota, Klein, Marieke, Knol, Maria J., Launer, Lenore J., Lawrie, Stephen M., Hellard, Stephanie Le, Lee, Phil H., Lemaître, Hervé, Li, Shuo, Liewald, David C. M., Lin, Honghuang, Longstreth, Jr, W. T., Lopez, Oscar L., Luciano, Michelle, Maillard, Pauline, Marquand, Andre F., Martin, Nicholas G., Martinot, Jean-Luc, Mather, Karen A., Mattay, Venkata S., McMahon, Katie L., Mecocci, Patrizia, Melle, Ingrid, Meyer-Lindenberg, Andreas, Mirza-Schreiber, Nazanin, Milaneschi, Yuri, Mosley, Thomas H., Mühleisen, Thomas W., Müller-Myhsok, Bertram, Maniega, Susana Muñoz, Nauck, Matthias, Nho, Kwangsik, Niessen, Wiro J., Nöthen, Markus M., Nyquist, Paul A., Oosterlaan, Jaap, Pandolfo, Massimo, Paus, Tomas, Pausova, Zdenka, Penninx, Brenda W. J. H., Pike, G. Bruce, Psaty, Bruce M., Pütz, Benno, Reppermund, Simone, Rietschel, Marcella D., Risacher, Shannon L., Romanczuk-Seiferth, Nina, Romero-Garcia, Rafael, Roshchupkin, Gennady V., Rotter, Jerome I., Sachdev, Perminder S., Sämann, Philipp G., Saremi, Arvin, Sargurupremraj, Muralidharan, Saykin, Andrew J., Schmaal, Lianne, Schmidt, Helena, Schmidt, Reinhold, Schofield, Peter R., Scholz, Markus, Schumann, Gunter, Schwarz, Emanuel, Shen, Li, Shin, Jean, Sisodiya, Sanjay M., Smith, Albert V., Smoller, Jordan W., Soininen, Hilkka S., Steen, Vidar M., Stein, Dan J., Stein, Jason L., Thomopoulos, Sophia I., Toga, Arthur W., Tordesillas-Gutiérrez, Diana, Trollor, Julian N., Valdes-Hernandez, Maria C., van ′t Ent, Dennis, van Bokhoven, Hans, van der Meer, Dennis, van der Wee, Nic J. A., Vázquez-Bourgon, Javier, Veltman, Dick J., Vernooij, Meike W., Villringer, Arno, Vinke, Louis N., Völzke, Henry, Walter, Henrik, Wardlaw, Joanna M., Weinberger, Daniel R., Weiner, Michael W., Wen, Wei, Westlye, Lars T., Westman, Eric, White, Tonya, Witte, A. Veronica, Wolf, Christiane, Yang, Jingyun, Zwiers, Marcel P., Ikram, M. Arfan, Seshadri, Sudha, Thompson, Paul M., Satizabal, Claudia L., Medland, Sarah E., and Rentería, Miguel E.

Published
2024
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6. Multi-parametric atlas of the pre-metastatic liver for prediction of metastatic outcome in early-stage pancreatic cancer

Author

Bojmar, Linda, Zambirinis, Constantinos P., Hernandez, Jonathan M., Chakraborty, Jayasree, Shaashua, Lee, Kim, Junbum, Johnson, Kofi Ennu, Hanna, Samer, Askan, Gokce, Burman, Jonas, Ravichandran, Hiranmayi, Zheng, Jian, Jolissaint, Joshua S., Srouji, Rami, Song, Yi, Choubey, Ankur, Kim, Han Sang, Cioffi, Michele, van Beek, Elke, Sigel, Carlie, Jessurun, Jose, Velasco Riestra, Paulina, Blomstrand, Hakon, Jönsson, Carolin, Jönsson, Anette, Lauritzen, Pernille, Buehring, Weston, Ararso, Yonathan, Hernandez, Dylanne, Vinagolu-Baur, Jessica P., Friedman, Madison, Glidden, Caroline, Firmenich, Laetitia, Lieberman, Grace, Mejia, Dianna L., Nasar, Naaz, Mutvei, Anders P., Paul, Doru M., Bram, Yaron, Costa-Silva, Bruno, Basturk, Olca, Boudreau, Nancy, Zhang, Haiying, Matei, Irina R., Hoshino, Ayuko, Kelsen, David, Sagi, Irit, Scherz, Avigdor, Scherz-Shouval, Ruth, Yarden, Yosef, Oren, Moshe, Egeblad, Mikala, Lewis, Jason S., Keshari, Kayvan, Grandgenett, Paul M., Hollingsworth, Michael A., Rajasekhar, Vinagolu K., Healey, John H., Björnsson, Bergthor, Simeone, Diane M., Tuveson, David A., Iacobuzio-Donahue, Christine A., Bromberg, Jaqueline, Vincent, C. Theresa, O’Reilly, Eileen M., DeMatteo, Ronald P., Balachandran, Vinod P., D’Angelica, Michael I., Kingham, T. Peter, Allen, Peter J., Simpson, Amber L., Elemento, Olivier, Sandström, Per, Schwartz, Robert E., Jarnagin, William R., and Lyden, David

Published
2024
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7. Tumour immune characterisation of primary triple-negative breast cancer using automated image quantification of immunohistochemistry-stained immune cells

Author

Suze Roostee, Daniel Ehinger, Mats Jönsson, Bengt Phung, Göran Jönsson, Gottfrid Sjödahl, Johan Staaf, and Mattias Aine

Subjects
Medicine, Science
Abstract

Abstract The tumour immune microenvironment (TIME) in breast cancer is acknowledged with an increasing role in treatment response and prognosis. With a growing number of immune markers analysed, digital image analysis may facilitate broader TIME understanding, even in single-plex IHC data. To facilitate analyses of the latter an open-source image analysis pipeline, Tissue microarray MArker Quantification (TMArQ), was developed and applied to single-plex stainings for p53, CD3, CD4, CD8, CD20, CD68, FOXP3, and PD-L1 (SP142 antibody) in a 218-patient triple negative breast cancer (TNBC) cohort with complementary pathology scorings, clinicopathological, whole genome sequencing, and RNA-sequencing data. TMArQ’s cell counts for analysed immune markers were on par with results from alternative methods and consistent with both estimates from human pathology review, different quantifications and classifications derived from RNA-sequencing as well as known prognostic patterns of immune response in TNBC. The digital cell counts demonstrated how immune markers are coexpressed in the TIME when considering TNBC molecular subtypes and DNA repair deficiency, and how combination of immune status with DNA repair deficiency status can improve the prognostic stratification in chemotherapy treated patients. These results underscore the value and potential of integrating TIME and specific tumour intrinsic alterations/phenotypes for the molecular understanding of TNBC.

Published
2024
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16. SGLT2 inhibition improves coronary flow velocity reserve and contractility: role of glucagon signaling

Author

Sven O. Göpel, Damilola Adingupu, Jue Wang, Elizaveta Semenova, Margareta Behrendt, Rasmus Jansson-Löfmark, Christine Ahlström, Ann-Cathrine Jönsson-Rylander, V. Sashi Gopaul, Russell Esterline, Li-Ming Gan, and Rui-Ping Xiao

Subjects
Metabolic syndrome, Heart failure, SGLT2 inhibitor, Coronary flow velocity reserve, Cardiac contractility, Glucagon, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract

Abstract Background SGLT2 inhibitors, a T2DM medication to lower blood glucose, markedly improve cardiovascular outcomes but the underlying mechanism(s) are not fully understood. SGLT2i’s produce a unique metabolic pattern by lowering blood glucose without increasing insulin while increasing ketone body and glucagon levels and reducing body weight. We tested if glucagon signaling contributes to SGLT2i induced improvement in CV function. Methods Cardiac contractility and coronary flow velocity reserve (CFVR) were monitored in ob/ob mice and rhesus monkeys with metabolic syndrome using echocardiography. Metabolic status was characterized by measuring blood ketone levels, glucose tolerance during glucose challenge and Arg and ADMA levels were measured. Baysian models were developed to analyse the data. Results Dapagliflozin improved CFVR and contractility, co-application of a glucagon receptor inhibitor (GcgRi) blunted the effect on CFVR but not contractility. Dapagliflozin increased the Arg/ADMA ratio and ketone levels and co-treatment with GcgRi blunted only the Dapagliflozin induced increase in Arg/ADMA ratio but not ketone levels. Conclusions Since GcgRi co-treatment only reduced the Arg/ADMA increase we hypothesize that dapagliflozin via a glucagon-signaling dependent pathway improves vascular function through the NO-signaling pathway leading to improved vascular function. Increase in ketone levels might be a contributing factor in SGLT2i induced contractility increase and does not require glucagon signaling. Graphical Abstract

Published
2024
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17. New connections of medication use and polypharmacy with the gut microbiota composition and functional potential in a large population

Author

Anna Larsson, Ulrika Ericson, Daniel Jönsson, Mariam Miari, Paschalis Athanasiadis, Gabriel Baldanzi, Louise Brunkwall, Sophie Hellstrand, Björn Klinge, Olle Melander, Peter M. Nilsson, Tove Fall, Marlena Maziarz, and Marju Orho-Melander

Subjects
Gut microbiota, Gut metabolic modules, Medications, Polypharmacy, Population cohort, Shotgun metagenomics, Medicine, Science
Abstract

Abstract Medication can affect the gut microbiota composition and function. The aim of this study was to investigate connections between use of common non-antibiotic medicines and the gut microbiota composition and function in a large Swedish cohort (N = 2223). Use of 67 medications and polypharmacy (≥ 5 medications), based on self-reported and prescription registry data, were associated with the relative abundance of 881 gut metagenomic species (> 5% prevalence) and 103 gut metabolic modules (GMMs). Altogether, 97 associations of 26 medications with 40 species and of four medications with five GMMs were observed (false discovery rate

Published
2024
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18. Double-layer optical fiber interferometer with bio-layer-modified reflector for label-free biosensing of inflammatory proteins

Author

Dariusz Burnat, Monika Janik, Norbert Kwietniewski, Agnieszka Martychowiec, Paulina Musolf, Krzysztof Bartnik, Marcin Koba, Tomasz P. Rygiel, Joanna Niedziółka-Jönsson, and Mateusz Śmietana

Subjects
Interferometry, Thin film, Optical fiber sensor, Label-free biosensing, Inflammatory protein, Myeloperoxidase, Medicine, Science
Abstract

Abstract This work discusses label-free biosensing application of a double-layer optical fiber interferometer where the second layer tailors the reflection conditions at the external plain and supports changes in reflected optical spectrum when a bio-layer binds to it. The double-layer nanostructure consists of precisely tailored thin films, i.e., titanium (TiO2) and hafnium oxides (HfO2) deposited on single-mode fiber end-face by magnetron sputtering. It has been shown numerically and experimentally that the approach besides well spectrally defined interference pattern distinguishes refractive index (RI) changes taking place in a volume and on the sensor surface. These are of interest when label-free biosensing applications are considered. The case of myeloperoxidase (MPO) detection—a protein, which concentration rises during inflammation—is reported as an example of application. The response of the sensor to MPO in a concentration range of 1 × 10−11–5 × 10−6 g/mL was tested. An increase in the MPO concentration was followed by a redshift of the interference pattern and a decrease in reflected power. The negative control performed using ferritin proved specificity of the sensor. The results reported in this work indicate capability of the approach for diagnostic label-free biosensing, possibly also at in vivo conditions.

Published
2024
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19. Caudate nucleus volume in medicated and unmedicated patients with early- and adult-onset schizophrenia

Author

Dimitrios Andreou, Kjetil Nordbø Jørgensen, Stener Nerland, Tereza Calkova, Lynn Mørch-Johnsen, Runar Elle Smelror, Laura A. Wortinger, Mathias Lundberg, Hannes Bohman, Anne Margrethe Myhre, Erik G. Jönsson, Ole A. Andreassen, and Ingrid Agartz

Subjects
Caudate, MRI, Schizophrenia, Early-onset, Adult-onset, Antipsychotics, Medicine, Science
Abstract

Abstract The caudate nucleus is a part of the striatum, and striatal hyperdopaminergia is considered central to the pathophysiology of schizophrenia. How caudate volume is affected in schizophrenia and what role antipsychotics play remains unclear. In early-onset schizophrenia (EOS), where psychosis emerges during a neurodevelopmentally critical phase, the caudate may exhibit a heightened vulnerability to the effects of antipsychotic medications. We hypothesized effects of both antipsychotic medication use and age of onset on caudate in schizophrenia. We included adult patients with EOS (n = 83) and adult-onset schizophrenia (AOS) (n = 246), adult healthy controls (HC, n = 774), adolescent patients with non-affective psychosis (n = 56) and adolescent HC (n = 97). We obtained T1-weighted MRI scans using a 1.5T Siemens scanner and General Electric 3T scanners. In our main analysis, we tested for main and interaction effects of diagnosis and current antipsychotic medication use on caudate volume. Adult patients with EOS (p

Published
2024
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20. Effects of a Paleolithic diet compared to a diabetes diet on leptin binding inhibition in secondary analysis of a randomised cross-over study

Author

Maelán Fontes-Villalba, Yvonne Granfeldt, Kristina Sundquist, Ashfaque A. Memon, Anna Hedelius, Pedro Carrera-Bastos, and Tommy Jönsson

Subjects
Paleolithic diet, Type 2 diabetes, Leptin, Leptin resistance, Wheat gluten, BioLep, Diseases of the endocrine glands. Clinical endocrinology, RC648-665
Abstract

Abstract Background Beneficial effects from practising a Paleolithic diet as compared to a diabetes diet on weight, waist circumference, satiety, leptin, HbA1c and glucose control in randomised controlled trial participants with type 2 diabetes could be due to lower leptin resistance. Support for this hypothesis comes from an in vitro experiment that showed that digested wheat gluten, which is excluded from a Paleolithic diet, inhibits leptin from binding to its receptor, thus indicating a possible dietary cause of leptin resistance. However, the clinical relevance of the latter finding is unclear since removal of enzyme activity from the gluten digest by heat treatment also abolished leptin binding inhibition. Assessment of leptin binding inhibition in vivo is possible by comparison of total leptin levels with those of ‘biologically active’ leptin bound to its receptor (bioLep). Objectives To assess the effects of a Paleolithic diet compared to a diabetes diet on leptin binding inhibition and to replicate our in vitro study. Methods BioLep and total leptin levels were measured in secondary analysis of fasting plasma samples from our open label random order three plus three-month long cross-over trial performed in 2005–2007, that compared a Paleolithic diet with a diabetes diet in participants with type 2 diabetes without insulin treatment (per protocol). BioLep was also measured in vitro for known recombinant leptin concentrations incubated with a series of concentrations of 10 kDa spin-filtered digested wheat gluten, with or without prior heat treatment, at 100ºC for 30 min and centrifugation. Results There was no difference between diets when comparing differences between bioLep and total leptin levels and their ratio in the 13 participants, three women and 10 men, aged 52–74 years with a mean BMI of 30 kg/m2 and a mean diabetes duration of eight years. We found no carry-over or period effect for bioLep and total leptin. In vitro, wheat gluten digest inhibited leptin binding in a dose-dependent manner but not after heat treatment. Conclusions We found no leptin binding inhibition after the Paleolithic or diabetes diet, possibly due to its abolishment from cooking-related heat treatment of wheat gluten. Trial registration Registered on 14/02/2007 at ClinicalTrials.gov Identifier: NCT00435240.

Published
2024
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21. GATA3 and markers of epithelial-mesenchymal transition predict long-term benefit from tamoxifen in ER-positive breast cancer

Author

Josefine Sandström, Jens Bomanson, Gizeh Pérez-Tenorio, Carolin Jönsson, Bo Nordenskjöld, Tommy Fornander, Linda S. Lindström, and Olle Stål

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract GATA binding protein 3 (GATA3) is essential for normal development of the mammary gland and associated with ER-positive breast cancer. Loss of GATA3 has been associated with epithelial-mesenchymal transition (EMT) in experimental studies. We investigated tumoral GATA3 in a cohort of postmenopausal patients with lymph-node negative breast cancer, randomized to adjuvant tamoxifen or control. Nuclear GATA3 expression was assessed with immunohistochemistry and GATA3 gene expression with Agilent microarrays. High GATA3 nuclear expression was associated with a lower rate of distant recurrence in ER-positive breast cancer (HR = 0.60, 95% CI 0.39–0.93). Low gene expression of GATA3 was associated with limited long-term benefit from adjuvant tamoxifen (interaction: p = 0.033). GATA3 gene expression was associated with the epithelial markers CDH1 (E-cadherin) and FOXA1, whereas negatively associated with several mesenchymal markers. Low expression of CDH1 was associated with marginal tamoxifen benefit (HR = 0.80 (0.43–1.49)), whereas patients with higher expression showed a significant benefit (HR = 0.33 (0.20–0.55), interaction: p = 0.029). In ER-positive breast cancer, diminished expression of GATA3 is associated with markers of EMT and poor long-term benefit from tamoxifen.

Published
2024
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45. Validation, Deployment, and Real-World Implementation of a Modular Toolbox for Alzheimer’s Disease Detection and Dementia Risk Reduction: The AD-RIDDLE Project

Author

Malzbender, K., Barbarino, P., Ferrell, P. Barkman, Bradshaw, A., Brookes, A. J., Díaz, C., van der Flier, W. M., Georges, J., Hansson, O., Hartmanis, M., Jönsson, L., Krishnan, R., MacLeod, T., Mangialasche, F., Mecocci, P., Minguillon, C., Middleton, L., Pla, S., Sardi, S. P., Schöll, M., Suárez-Calvet, M., Weidner, W., Visser, P. J., Zetterberg, H., Bose, N., Solomon, A., and Kivipelto, Miia

Published
2024
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49. DNA methylation governs the sensitivity of repeats to restriction by the HUSH-MORC2 corepressor

Author

Ninoslav Pandiloski, Vivien Horváth, Ofelia Karlsson, Symela Koutounidou, Fereshteh Dorazehi, Georgia Christoforidou, Jon Matas-Fuentes, Patricia Gerdes, Raquel Garza, Marie E. Jönsson, Anita Adami, Diahann A. M. Atacho, Jenny G. Johansson, Elisabet Englund, Zaal Kokaia, Johan Jakobsson, and Christopher H. Douse

Subjects
Science
Abstract

Abstract The human silencing hub (HUSH) complex binds to transcripts of LINE-1 retrotransposons (L1s) and other genomic repeats, recruiting MORC2 and other effectors to remodel chromatin. How HUSH and MORC2 operate alongside DNA methylation, a central epigenetic regulator of repeat transcription, remains largely unknown. Here we interrogate this relationship in human neural progenitor cells (hNPCs), a somatic model of brain development that tolerates removal of DNA methyltransferase DNMT1. Upon loss of MORC2 or HUSH subunit TASOR in hNPCs, L1s remain silenced by robust promoter methylation. However, genome demethylation and activation of evolutionarily-young L1s attracts MORC2 binding, and simultaneous depletion of DNMT1 and MORC2 causes massive accumulation of L1 transcripts. We identify the same mechanistic hierarchy at pericentromeric α-satellites and clustered protocadherin genes, repetitive elements important for chromosome structure and neurodevelopment respectively. Our data delineate the epigenetic control of repeats in somatic cells, with implications for understanding the vital functions of HUSH-MORC2 in hypomethylated contexts throughout human development.

Published
2024
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50. Neck muscle function improves after neck exercises in individuals with whiplash-associated disorders: a case–control ultrasound study with speckle-tracking analyses

Author

Gunnel Peterson, David Nilsson, Margaretha Jönsson, Kate Bennett, and Anneli Peolsson

Subjects
Whiplash injury, Ultrasonography, Neck muscles, Spine, Rehabilitation, Physical therapy, Medicine, Science
Abstract

Abstract A whiplash injury can alter neck muscle function, which remains years after the injury and may explain why symptoms such as persistent pain and disability occur. There is currently limited knowledge about dynamic neck muscle function in chronic whiplash-associated disorders (WAD), and about the extent to which altered muscle function can improve after rehabilitation. Ultrasound can detect mechanical neck muscle function by measuring real-time deformation and deformation rate in the muscles. This method was used for five dorsal neck muscles in participants with chronic WAD versus matched controls in resistant neck rotation. We obtained real-time, non-invasive ultrasound measurements using speckle tracking, multivariate analyses, and mixed-design ANOVA analyses. The results showed altered deformation in the three deepest neck muscle layers, with less deformation area in the WAD group compared to controls in rotation to the most painful side at baseline. Participants in the WAD group performed three months of neck-specific exercises, resulting in improved deformation in the deep neck muscles in WAD and with a similar deformation pattern to controls, and the significant group differences ceased. We reveal new and important insights into the capability of ultrasound to diagnose altered neck muscle function and evaluate an exercise intervention.

Published
2024
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