tbuckley/cabot-search huggingface dataset:
TCT-178 Intravascular Ultrasound Predictors of Long-Term Outcomes Following ABSORB Bioresorbable Scaffold Implantation: A Pooled Analysis of the ABSORB III and ABSORB Japan Trials
Authors: Takeshi Nishi, Kozo Okada, Hideki Kitahara, Masayasu Ikutomi, M. Brooke Hollak, Paul G. Yock, Jeffrey Popma, Hajime Kusano, Wai-Fung Cheong, Krishna Sudhir, Stephen Ellis, Dean Kereiakes, Gregg Stone, Yasuhiro Honda, Takeshi Kimura
Journal: Journal of the American College of Cardiology (2019)
TCT-586 Association Between Renal Function and Fractional Flow Reserve: Data From a Prospective IRIS-FFR Registry (Interventional Cardiology Research Incooperation Society Fractional Flow Reserve)
Authors: Ha-Wook Park, Sung-Ho Her, Jong Bum Kwon, Ji Su Mok, Duk-Woo Park, Bon-Kwon Koo, Chang-Wook Nam, Joon-Hyung Doh, Seung-Jung Park
Journal: Journal of the American College of Cardiology (2019)
PBK/TOPK, a mitotic Ser/Thr kinase, is a novel druggable target for breast cancer therapy
Authors: Jae-Hyun Park, Toyomasa Katagiri, Yusuke Nakamura
Journal: Cancer Research (2008)

2364  Breast cancer is the most common cancer among women worldwide. However, since the precise molecular mechanisms driving breast cancer are still not fully understood, treatment to the patients at an advanced stage is limited. To discover novel therapeutic targets for breast cancer, we previously performed the detailed genome-wide expression profile analysis of 81 breast cancers by a combination of laser microbeam microdissection and cDNA microarrays. Among the transactivated genes in breast cancer, we identified a breast cancer-specific Ser/Thr protein kinase, PBK/TOPK (PDZ-binding kinase/T-LAK cell-originated protein kinase). Northern blot analysis and immunohistochemical analyses with anti-PBK/TOPK monoclonal antibody confirmed that PBK/TOPK is up-regulated in great majority of breast cancer cells, whereas its expression was not or hardly detectable in normal human organs examined except testis, indicating it to be a typical cancer/testis antigen. Its over expression was observed in three different histological subtypes of breast cancer including intraductal, papillo-tubular, and scirrhous carcinomas. PBK/TOPK was specifically up-regulated and autophosphorylated during cell mitosis, suggesting its critical role in unrestrained mitosis of cancer cells. Moreover, the PBK/TOPK gene-depletion by siRNA resulted in the increased population of apoptotic cells as well as cytokinetic defects in breast cancer cell-lines, T47D and ZR-75-1. Time-lapse microscopy also identified incomplete abscission of dividing cells and delayed cytokinesis in the PBK/TOPK-depleted breast cancer cells. These findings suggest that PBK/TOPK functions as a mitotic kinase, and is indispensable for breast cancer cell growth.
HBx Protein Contributes to Liver Carcinogenesis by H3K4me3 Modification Through Stabilizing WD Repeat Domain 5 Protein
Authors: Weiwu Gao, Zhengcai Jia, Yi Tian, Penghui Yang, Hui Sun, Chenhui Wang, Yi Ding, Mengjie Zhang, Yi Zhang, Di Yang, Zhiqiang Tian, Jian Zhou, Zhihua Ruan, Yuzhang Wu, Bing Ni
Journal: Hepatology (2019)

Cancer is typically considered as a genetic and epigenetic disease. Although numerous studies have indicated that an aberrant structure, function, or expression level of epigenetic enzymes contribute to many tumor types, precisely how the epigenetic mechanisms are involved in the hepatitis B virus (HBV)-induced hepatocellular carcinoma (HCC) remains unknown.In this study, we found that the WD repeat domain 5 protein (WDR5)-a core subunit of histone H3 lysine 4 methyltransferase complexes, which catalyze the generation of histone H3 lysine 4 trimethylation (H3K4me3) modification-is highly expressed in HBV-related HCC and promotes HCC development. WDR5 plays a critical role in HBV-driven cell proliferation and tumor growth in mice, and the WDR5-0103 small-molecule inhibitor of WDR5 activity compromises HBV- and hepatitis B x protein (HBx)-driven tumor proliferation. The aberrantly high WDR5 protein level was found to involve HBx through its stabilization of the WDR5 protein by inhibiting the interaction between the damage-specific DNA-binding protein 1/cullin-4 and WDR5, causing decreased ubiquitination of the WDR5 protein. HBx was found to colocalize with WDR5 on chromatin genome wide and promotes genome-wide H3K4me3 modification by means of WDR5. Furthermore, the recruitment of HBx to promoters of target genes relied on its interaction with WDR5 through its α-helix domain. WDR5 was also found to promote HBV transcription through H3K4 modification of covalently closed circular DNA minichromosome, and WDR5-0103 was able to inhibit HBV transcription. Finally, the in vitro and in vivo data further proved that HBx exerted its tumor-promoting function in a WDR5-dependent manner.Our data reveals that WDR5 is a key epigenetic determinant of HBV-induced tumorigenesis and that the HBx-WDR5-H3K4me3 axis may be a potential therapeutic target in HBV-induced liver pathogenesis.
TCT-666 Percutaneous Coronary Intervention in In-Stent Restenosis Lesions With Second-Generation Drug Coated Balloons: Results at a Long-Term Follow-Up
Authors: Ignacio Sanchez-Perez, José Abellán-Huerta, María López-Lluva, Pedro Pérez-Díaz, Jesus Piqueras-Flores, Ramón Maseda Uriza, Juan Antonio Requena, Alfonso Jurado-Román, Fernando Lozano
Journal: Journal of the American College of Cardiology (2019)
Abstract #5284: Interaction of estrogen with stimulating and inhibiting signaling pathways of lung adenocarcinoma
Authors: Mourad Majidi, Hussein Al-Wadei, Hildegard Schüller
Journal: Cancer Research (2009)

Small airway-derived pulmonary adenocarcinoma (PAC) is the leading type of lung cancer today and women are at a higher risk than men to develop PAC. We have shown that the nicotine-derived nitrosamine NNK stimulates the growth and migration of PAC cells in vitro by cAMP-mediated signaling downstream of \#946;1-adrenoreceptors (\#946;1-ARs) and that estrogen enhances the effectiveness of this pathway by signaling via the estrogen receptor beta (ER\#946;). Our current data demonstrate that the observed cooperation between NNK and estrogen-induced stimulating signaling in the cells of origin of PAC involves the formation of a \#946;1-AR/ER\#946; complex. Transfection with oncogenic Ras12V enhanced this cooperative signaling while transfection with dominant negative 17N Ras blocked this pathway. Transfection of cells with the regulator of G-protein signaling 5 (RGS5) reduced while blockade of the inhibitory G-protein G\#945;1 by pertussis toxin (PTX) significantly enhanced signaling responses. The neurotransmitter \#947;-aminobutyric acid (GABA) completely blocked cAMP formation and its downstream responses an effect mediated by the G\#945;i-coupled GABAB receptor. Studies are currently underway to investigate if chronic exposure to estrogen suppresses GABA in small airway epithelial cells. The resulting dual estrogenic influence on PAC development by enhaned \#946;1-AR signaling and deficient inhibitory GABA signaling would provide a pulmonary microenvironment that selectively supports the development of PAC in women. Supported by a contract with the National Lung Cancer Partnership.  Citation Information: In: Proc Am Assoc Cancer Res; 2009 Apr 18-22; Denver, CO. Philadelphia (PA): AACR; 2009. Abstract nr 5284.
Physical activity differs with sex and age
Authors: Liaquat R Johnson
Journal: BMJ (2019)

Ekelund and colleagues report a non-linear dose-response between all levels of physical activity and mortality.1 Their findings support guidance on physical activity from the World Health Organization.23

But I have some concerns. First, over 70% of study participants were women. Globally, women are less physically active than men across all ages.3 So the physical activity levels obtained in this study are less likely to be …
TCT-591 A Comparison of Clinical and Coronary Physiology Characteristics in Patients With and Without Type 4a Myocardial Infarction Following High Speed Rotational Atherectomy–Assisted Percutaneous Coronary Intervention
Authors: Damien Collison, David Corcoran, David Carrick, Kenneth Mangion, Barry Hennigan, Novalia Sidik, Tom Ford, Keith Robertson, Aadil Shaukat, Paul Rocchiccioli, Stuart Watkins, Mitchell Lindsay, Hany Eteiba, Keith Oldroyd, Colin Berry, Margaret McEntegart
Journal: Journal of the American College of Cardiology (2019)
TCT-608 Implementation of Bayesian Study Design in the SPYRAL HTN-OFF MED Pivotal Trial
Authors: Michael Böhm, Raymond Townsend, Michael Weber, David Kandzari, Felix Mahfoud, Kazuomi Kario, Roland Schmieder, Konstantinos Tsioufis, Vanessa DeBruin, Graeme Hickey, Martin Fahy, Stuart Pocock
Journal: Journal of the American College of Cardiology (2019)
TCT-822 Culprit Vessel Only Versus Multivessel Percutaneous Coronary Intervention in Patients With NSTEMI and Cardiogenic Shock: Insights From the NCDR CathPCI Registry
Authors: Mohamed Omer, Emmanouil Brilakis, Kevin Kennedy, Islam Elgendy, Philip Jones, Jonathan Enriquez, Suzanne Arnold, Paul Chan, John Spertus
Journal: Journal of the American College of Cardiology (2019)
Repurposing quinacrine for treatment-refractory cancer
Authors: Derek B. Oien, Christopher L. Pathoulas, Upasana Ray, Prabhu Thirusangu, Eleftheria Kalogera, Viji Shridhar
Journal: Seminars in Cancer Biology (2019)

Quinacrine, also known as mepacrine, has originally been used as an antimalarial drug for close to a century, but was recently rediscovered as an anticancer agent. The mechanisms of anticancer effects of quinacrine are not well understood. The anticancer potential of quinacrine was discovered in a screen for small molecule activators of p53, and was specifically shown to inhibit NFκB suppression of p53. However, quinacrine can cause cell death in cells that lack p53 or have p53 mutations, which is a common occurrence in many malignant tumors including high grade serous ovarian cancer. Recent reports suggest quinacrine may inhibit cancer cell growth through multiple mechanisms including regulating autophagy, FACT (facilitates chromatin transcription) chromatin trapping, and the DNA repair process. Additional reports also suggest quinacrine is effective against chemoresistant gynecologic cancer. In this review, we discuss anticancer effects of quinacrine and potential mechanisms of action with a specific focus on gynecologic and breast cancer where treatment-refractory tumors are associated with increased mortality rates. Repurposing quinacrine as an anticancer agent appears to be a promising strategy based on its ability to target multiple pathways, its selectivity against cancer cells, and the synergistic cytotoxicity when combined with other anticancer agents with limited side effects and good tolerability profile.
Abstract 14123: Interventricular Dyssynchrony Using Cine-Tagging MRI in Adult Congenital Heart Disease: Prediction of Right Ventricular Dysfunction
Authors: Michinobu Nagao, Masato Yonezawa, Yoshio Matsuo, Takeshi Kamitani, Mikako Jinnouchi, Yuzo Yamasaki, Ko Higuchi, Kenichiro Yamamura, Kohtaro Abe, Ichiro Sakamoto, Hiroshi Honda
Journal: Circulation (2012)

PURPOSE: Right ventricular (RV) failure and ventricular dyssynchrony are strong determinants of prognosis in patients with adult congenital heart disease (ACHD). Although mechanical dyssynchrony us...
TCT-260 Procedural Optimization Improved the Clinical Outcome of Drug-Coated Balloon for DES-ISR: Proposal of the “DCB 4 Factors”
Authors: Jeehoon Kang, Hak Seung Lee, You Jeong Ki, Jung-Kyu Han, Han-Mo Yang, Kyung Woo (K.W.) Park, Hyun-Jae Kang, Bon-Kwon Koo, Hyo-Soo Kim
Journal: Journal of the American College of Cardiology (2019)
TCT-265 Percutaneous Coronary Interventions With Drug-Coated Balloons or Drug-Eluting Stents for the Treatment of Small Native Vessel Coronary Artery Disease: A Meta-Analysis of Randomized Trials
Authors: Jorge Sanz Sanchez, Mauro Chiarito, Andrea Moretti, Damiano Regazzoli, Paolo Pagnotta, Bernhard Reimers, Giulio Stefanini, Giuseppe Ferrante
Journal: Journal of the American College of Cardiology (2019)
TCT-488 Time-to-Telemedicine Diagnosis, A New Metric in STEMI Interventions
Authors: Sameer Mehta, Roberto Botelho, Jamil Cade, Marco Perin, Mauricio Prudente, Ricardo Cavalcanti, Cesar Dusilek, Rodolfo Cardoso, Nabil Hamdan, Luis Ignacio Calderon, Marco Alcocer-Gamba, Juan Carlos Perez Alva, Alfredo Estrada, Manuel De Los Rios Ibarra, Alejandro Ricalde, Alejandra Frauenfelder, Daniel Vieira, Mariana Ceschim, Gladys Pinto, Rodrigo Jacobucci, Francisco Nola, Seyna Krisciunas, Isabella Vallenilla, Maritza Luna, Daniela Bou Daher, Akhil Vaid
Journal: Journal of the American College of Cardiology (2019)
The 2019 USPSTF Report on Screening for Asymptomatic Bacteriuria—Lessons From History
Authors: Kalpana Gupta, Barbara W. Trautner
Journal: JAMA Network Open (2019)

US Preventive Services Task Force; Douglas K. Owens, MD, MS; Karina W. Davidson, PhD, MASc; Alex H. Krist, MD, MPH; Michael J. Barry, MD; Michael Cabana, MD, MA, MPH; Aaron B. Caughey, MD, PhD; Chyke A. Doubeni, MD, MPH; John W. Epling Jr, MD, MSEd; Martha Kubik, PhD, RN; C. Seth Landefeld, MD; Carol M. Mangione, MD, MSPH; Lori Pbert, PhD; Michael Silverstein, MD, MPH; Melissa A. Simon, MD, MPH; Chien-Wen Tseng, MD, MPH, MSEE; John B. Wong, MD
TCT-206 Conservative Versus Aggressive Treatment Strategy With Angiographic Guidance Alone in Patients With Intermediate Coronary Lesions: 3-Year Outcome of the SMART-CASE Trial
Authors: Kim Jihoon, Joo-Yong Hahn, Kyutae Park, Young Bin Song, Jin-Ho Choi, Seung-Hyuk Choi, Hyeon-Cheol Gwon
Journal: Journal of the American College of Cardiology (2019)
TCT-402 Optimal Duration of Antiplatelet therapy After Drug-Eluting Stent Implantation Based on PRECISE-DAPT and DAPT Scores
Authors: Ji-Yong Jang, Byoung Kwon Lee, Jung-Sun Kim, Myeong-Ki Hong, Kyung Woo (KW) Park, Hyo-Soo Kim, Hyuck Moon Kwon, Yangsoo Jang
Journal: Journal of the American College of Cardiology (2019)
A good doctor is empathetic to all
Authors: Yang Chen
Journal: BMJ (2019)

In searching for what it means to be a good doctor,1 we must ask and engage with those who are on the receiving end of our care.

A systematic review of patients’ priorities conducted two decades ago found that “humaneness,” “competence/accuracy,” and “involvement in decision making” were important markers of good care.2 Similar priorities were reported in a more …
A Deactivation Factor of Fibrogenic Hepatic Stellate Cells Induces Regression of Liver Fibrosis in Mice
Authors: Yasuhiro Nakano, Akihide Kamiya, Hideaki Sumiyoshi, Kota Tsuruya, Tatehiro Kagawa, Yutaka Inagaki
Journal: Hepatology (2019)

Background and Aims Hepatic stellate cells (HSCs), a key player in the progression of liver fibrosis, are activated by various inflammatory stimuli and converted to myofibroblast‐like cells with excessive collagen production. Despite many attempts to suppress activation of HSCs or inhibit collagen production in activated HSCs, their clinical applications have not been established yet. Recently, the deactivation of HSCs has been reported as a mechanism underlying the reversibility of experimental liver fibrosis. In the present study, we sought for deactivation factors of HSCs that induce regression of established liver fibrosis. Approach and Results We identified transcription factor 21 (Tcf21) as one of the transcription factors whose expression was up‐regulated in parallel to the differentiation of fetal HSCs. Expression of Tcf21 in HSCs remarkably decreased during culture‐induced activation in vitro and in murine and human fibrotic liver tissue in vivo . This reduced Tcf21 expression was recovered during the spontaneous regression of murine liver fibrosis. Tcf21 was also examined for its effects by adeno‐associated virus serotype 6‐mediated Tcf21 gene transfer into cultured activated HSCs and mice with carbon tetrachloride‐ or methionine‐choline deficient diet‐induced liver fibrosis. Overexpression of Tcf21 in activated HSCs not only suppressed fibrogenic gene expression but also restored cells, at least in part, to a quiescent phenotype both in vitro and in vivo . These phenotypic changes of HSCs were accompanied by the regression of steatohepatitis and fibrosis and improved hepatic architecture and function. Conclusions Tcf21 has been identified as a deactivation factor of fibrogenic HSCs, providing insight into a treatment strategy for the otherwise intractable liver fibrosis.
EWS-FLI1 interferes with p53-dependent growth control in Ewing´s sarcoma by suppressing autostimulation of the NOTCH pathway
Authors: Jozef Ban, Karl-Ludwig Schaefer, Michael Kreppel, Radostina Bachmaier, Heinrich Kovar
Journal: Cancer Research (2007)

2109  The EWS-FLI1 fusion oncoprotein is the driving force in the pathogenesis of Ewing´s sarcoma family tumors (ESFT). It acts as an aberrant transcriptional regulator conferring tumorigenic properties to several transfected cell types including bone marrow mesenchymal progenitor cells, and is required for sustained growth of ESFT cells in-vitro and in-vivo. Silencing of EWS-FLI1 expression in ESFT cell lines leads to growth arrest and eventually to cell death or senescence. We have observed transcriptional stimulation of p21CDKN1A expression in six wildtype p53 ESFT cell lines upon RNAi-mediated EWS-FLI1 silencing. This induction was p53 dependent. Among the genes upregulated by EWS-FLI1 suppression we identified the hairy enhancer of split (HES) family transcription factor gene HEY1, which has recently been shown to positively modulate p53 protein levels in human colon cancer HCT116 cells. In fact, silencing of EWS-FLI1 in ESFT cells resulted in p53 stabilization and Ser15 phosphorylation, which were inhibited by siRNA to HEY1. Since HES transcription factors are downstream effectors of NOTCH signalling, we investigated the expression and the activation status of NOTCH signalling components in ESFT cells before and after EWS-FLI1 knock-down by RNAi. A strong induction of the NOTCH ligand JAG1 and variable increases in the expression of NOTCH receptors 2 and 3 were consistently observed upon silencing of EWS-FLI1. Concomitantly, NOTCH pathway activation by gamma secretase dependent proteolytic receptor cleavage leading to nuclear translocation of the NOTCH intracellular domain (NICD) was detected. Modulation of JAG1 induction by specific siRNA and inhibition of NOTCH processing by either a chemical gamma secretase inhibitor or ectopic expression of the physiologic NOTCH inhibitory docking protein NUMB1 inhibited p53 and p21CDKN1A induction. These results indicate that suppression of EWS-FLI1 expression reactivates NOTCH signalling in ESFT resulting in p53 dependent cell cycle arrest. Gene expression profiling of 27 primary tumors and 12 cell lines revealed consistent expression of NOTCH2 by ESFT. Since ectopic JAG1 expression sufficed to activate the p53 checkpoint via NOTCH pathway stimulation, we hypothesize that homing of ESFT cells to a NOTCH ligand-expressing compartment like the trabecular bone and the bone marrow may slow-down ESFT growth, possibly providing a molecular basis for dormant disease and late relapse.  Supported by the Austrian Genome Research Programme GEN-AU (grant 200.136/1-VI/1/2005 GEN-AU-Ch.I.L.D.), the European commission (grant EC-FP6 STREP 503036 “PROTHETS”), and the Austrian Research Fund, grants 16067-B04 and 18046-B12.
TCT-349 Delineation of Ambiguous Coronary Lesions in Patients Undergoing Coronary Angiography for Acute Coronary Syndrome: Results From an Optical Coherence Tomography Study
Authors: Klio Konstantinou, Thomas Keeble, Osama Alsanjari, Kare Tang, Jeremy Sayer, Rajesh Aggarwal, Gerald Clesham, John Davies, Grigoris Karamasis
Journal: Journal of the American College of Cardiology (2019)
Primary ciliary dyskinesia patients have the same <i>P. aeruginosa</i> clone in sinuses and lungs
Authors: Elisabeth Arndal, Helle K. Johansen, Janus A.J. Haagensen, Jennifer A. Bartell, Rasmus L. Marvig, Mikkel Alanin, Kasper Aanæs, Niels Høiby, Kim G. Nielsen, Vibeke Backer, Christian von Buchwald
Journal: European Respiratory Journal (2019)

<b>For the first time it is shown that the same <i>Pseudomonas aeruginosa</i> clone exists in both the upper and lower airways in patients with PCD, providing a solid support of the unified airway theory where the sinuses are a possible bacterial reservoir</b>http://bit.ly/2kcE9tq
TCT-44 Impact of Stent Edge Hinging on Chronic Neointimal Hyperplasia After Newer-Generation Drug-Eluting Stent Placement in RCA
Authors: Takahiro Jimba, Masayasu Ikutomi, Masataka Yamasaki, Daigo Nishijyo, Akito Shindou, Kotaro Mochida, Tomoyoshi Yanagisawa, Takahiro Sato, Masashirou Matsushita, Satoru Ohnishi, Masao Yamasaki
Journal: Journal of the American College of Cardiology (2019)
A Highly Efficient and GMP Compliant Protocol to Manufacture CCR5 Edited Cells to Treat HIV Infection
Authors: Marianna Romito, Emily Meyer, Sushmita Poddar, Helena Heinz, Julia Rositzka, Markus Hildenbeutel, Anne-Sophie Gautron, Brian W Busser, Yik Lim Kok, Giandomenico Turchiano, Simone Haas, Richard Schäfer, Julianne Smith, Karin J Metzner, Claudio Mussolino, Philippe Duchateau, Toni Cathomen, Tatjana I Cornu
Journal: Blood (2018)
The Focal Adhesion Complex Ilk-Pinch-Parvin Is Key to Niche Interactions and Survival of Quiescent Stem Cells in Chronic Myeloid Leukemia In Vitro and In Vivo
Authors: Katharina Rothe, Artem Babaian, Naoto Nakamichi, Min Chen, Akie Watanabe, Dixie Mager, Connie J. Eaves, Shoukat Dedhar, Xiaoyan Jiang
Journal: Blood (2016)
Common brain disorders are associated with heritable patterns of apparent aging of the brain
Authors: Tobias Kaufmann, Dennis van der Meer, Nhat Trung Doan, Emanuel Schwarz, Martina J Lund, Ingrid Agartz, Dag Alnæs, Deanna M Barch, Ramona Baur-Streubel, Alessandro Bertolino, Francesco Bettella, Mona K Beyer, Erlend Bøen, Stefan Borgwardt, Christine L Brandt, Jan Buitelaar, Elisabeth G Celius, Simon Cervenka, Annette Conzelmann, Aldo Córdova-Palomera, Anders M Dale, Dominique J F de Quervain, Pasquale Di Carlo, Srdjan Djurovic, Erlend S Dørum, Sarah Eisenacher, Torbjørn Elvsåshagen, Thomas Espeseth, Helena Fatouros-Bergman, Lena Flyckt, Barbara Franke, Oleksandr Frei, Beathe Haatveit, Asta K Håberg, Hanne F Harbo, Catharina A Hartman, Dirk Heslenfeld, Pieter J Hoekstra, Einar A Høgestøl, Terry L Jernigan, Rune Jonassen, Erik G Jönsson, Peter Kirsch, Iwona Kłoszewska, Knut K Kolskår, Nils Inge Landrø, Stephanie Le Hellard, Klaus-Peter Lesch, Simon Lovestone, Arvid Lundervold, Astri J Lundervold, Luigi A Maglanoc, Ulrik F Malt, Patrizia Mecocci, Ingrid Melle, Andreas Meyer-Lindenberg, Torgeir Moberget, Linn B Norbom, Jan Egil Nordvik, Lars Nyberg, Jaap Oosterlaan, Marco Papalino, Andreas Papassotiropoulos, Paul Pauli, Giulio Pergola, Karin Persson, Geneviève Richard, Jaroslav Rokicki, Anne-Marthe Sanders, Geir Selbæk, Alexey A Shadrin, Olav B Smeland, Hilkka Soininen, Piotr Sowa, Vidar M Steen, Magda Tsolaki, Kristine M Ulrichsen, Bruno Vellas, Lei Wang, Eric Westman, Georg C Ziegler, Mathias Zink, Ole A Andreassen, Lars T Westlye
Journal: Nature Neuroscience (2019)