@article{SeboldChenOenaletal.2022, author = {Sebold, Miriam and Chen, Hao and {\"O}nal, Aleyna and Kuitunen-Paul, S{\"o}ren and Mojtahedzadeh, Negin and Garbusow, Maria and Nebe, Stephan and Wittchen, Hans-Ulrich and Huys, Quentin J. M. and Schlagenhauf, Florian and Rapp, Michael A. and Smolka, Michael N. and Heinz, Andreas}, title = {Stronger prejudices are associated with decreased model-based control}, series = {Frontiers in psychology}, volume = {12}, journal = {Frontiers in psychology}, publisher = {Frontiers Research Foundation}, address = {Lausanne}, issn = {1664-1078}, doi = {10.3389/fpsyg.2021.767022}, pages = {10}, year = {2022}, abstract = {Background: Prejudices against minorities can be understood as habitually negative evaluations that are kept in spite of evidence to the contrary. Therefore, individuals with strong prejudices might be dominated by habitual or "automatic" reactions at the expense of more controlled reactions. Computational theories suggest individual differences in the balance between habitual/model-free and deliberative/model-based decision-making. Methods: 127 subjects performed the two Step task and completed the blatant and subtle prejudice scale. Results: By using analyses of choices and reaction times in combination with computational modeling, subjects with stronger blatant prejudices showed a shift away from model-based control. There was no association between these decision-making processes and subtle prejudices. Conclusion: These results support the idea that blatant prejudices toward minorities are related to a relative dominance of habitual decision-making. This finding has important implications for developing interventions that target to change prejudices across societies.}, language = {en} } @article{ChanChaudharySahaetal.2021, author = {Chan, Lili and Chaudhary, Kumardeep and Saha, Aparna and Chauhan, Kinsuk and Vaid, Akhil and Zhao, Shan and Paranjpe, Ishan and Somani, Sulaiman and Richter, Felix and Miotto, Riccardo and Lala, Anuradha and Kia, Arash and Timsina, Prem and Li, Li and Freeman, Robert and Chen, Rong and Narula, Jagat and Just, Allan C. and Horowitz, Carol and Fayad, Zahi and Cordon-Cardo, Carlos and Schadt, Eric and Levin, Matthew A. and Reich, David L. and Fuster, Valentin and Murphy, Barbara and He, John C. and Charney, Alexander W. and B{\"o}ttinger, Erwin and Glicksberg, Benjamin and Coca, Steven G. and Nadkarni, Girish N.}, title = {AKI in hospitalized patients with COVID-19}, series = {Journal of the American Society of Nephrology : JASN}, volume = {32}, journal = {Journal of the American Society of Nephrology : JASN}, number = {1}, publisher = {American Society of Nephrology}, address = {Washington}, organization = {Mt Sinai COVID Informatics Ct}, issn = {1046-6673}, doi = {10.1681/ASN.2020050615}, pages = {151 -- 160}, year = {2021}, abstract = {Background: Early reports indicate that AKI is common among patients with coronavirus disease 2019 (COVID-19) and associatedwith worse outcomes. However, AKI among hospitalized patients with COVID19 in the United States is not well described. Methods: This retrospective, observational study involved a review of data from electronic health records of patients aged >= 18 years with laboratory-confirmed COVID-19 admitted to the Mount Sinai Health System from February 27 to May 30, 2020. We describe the frequency of AKI and dialysis requirement, AKI recovery, and adjusted odds ratios (aORs) with mortality. Results: Of 3993 hospitalized patients with COVID-19, AKI occurred in 1835 (46\%) patients; 347 (19\%) of the patientswith AKI required dialysis. The proportionswith stages 1, 2, or 3 AKIwere 39\%, 19\%, and 42\%, respectively. A total of 976 (24\%) patients were admitted to intensive care, and 745 (76\%) experienced AKI. Of the 435 patients with AKI and urine studies, 84\% had proteinuria, 81\% had hematuria, and 60\% had leukocyturia. Independent predictors of severe AKI were CKD, men, and higher serum potassium at admission. In-hospital mortality was 50\% among patients with AKI versus 8\% among those without AKI (aOR, 9.2; 95\% confidence interval, 7.5 to 11.3). Of survivors with AKI who were discharged, 35\% had not recovered to baseline kidney function by the time of discharge. An additional 28 of 77 (36\%) patients who had not recovered kidney function at discharge did so on posthospital follow-up. Conclusions: AKI is common among patients hospitalized with COVID-19 and is associated with high mortality. Of all patients with AKI, only 30\% survived with recovery of kidney function by the time of discharge.}, language = {en} } @article{ChenNebeMojtahedzadehetal.2020, author = {Chen, Hao and Nebe, Stephan and Mojtahedzadeh, Negin and Kuitunen-Paul, Soren and Garbusow, Maria and Schad, Daniel and Rapp, Michael A. and Huys, Quentin J. M. and Heinz, Andreas and Smolka, Michael N.}, title = {Susceptibility to interference between Pavlovian and instrumental control is associated with early hazardous alcohol use}, series = {Addiction biology}, volume = {26}, journal = {Addiction biology}, number = {4}, publisher = {Wiley}, address = {Hoboken}, issn = {1355-6215}, doi = {10.1111/adb.12983}, pages = {1 -- 14}, year = {2020}, abstract = {Pavlovian-to-instrumental transfer (PIT) tasks examine the influence of Pavlovian stimuli on ongoing instrumental behaviour. Previous studies reported associations between a strong PIT effect, high-risk drinking and alcohol use disorder. This study investigated whether susceptibility to interference between Pavlovian and instrumental control is linked to risky alcohol use in a community sample of 18-year-old male adults. Participants (N = 191) were instructed to 'collect good shells' and 'leave bad shells' during the presentation of appetitive (monetary reward), aversive (monetary loss) or neutral Pavlovian stimuli. We compared instrumental error rates (ER) and functional magnetic resonance imaging (fMRI) brain responses between the congruent and incongruent conditions, as well as among high-risk and low-risk drinking groups. On average, individuals showed a substantial PIT effect, that is, increased ER when Pavlovian cues and instrumental stimuli were in conflict compared with congruent trials. Neural PIT correlates were found in the ventral striatum and the dorsomedial and lateral prefrontal cortices (lPFC). Importantly, high-risk drinking was associated with a stronger behavioural PIT effect, a decreased lPFC response and an increased neural response in the ventral striatum on the trend level. Moreover, high-risk drinkers showed weaker connectivity from the ventral striatum to the lPFC during incongruent trials. Our study links interference during PIT to drinking behaviour in healthy, young adults. High-risk drinkers showed higher susceptibility to Pavlovian cues, especially when they conflicted with instrumental behaviour, indicating lower interference control abilities. Increased activity in the ventral striatum (bottom-up), decreased lPFC response (top-down), and their altered interplay may contribute to poor interference control in the high-risk drinkers.}, language = {en} } @article{XiongDelicZengetal.2022, author = {Xiong, Yingquan and Delic, Denis and Zeng, Shufei and Chen, Xin and Chu, Chang and Hasan, Ahmed A. and Kr{\"a}mer, Bernhard K. and Klein, Thomas and Yin, Lianghong and Hocher, Berthold}, title = {Regulation of SARS CoV-2 host factors in the kidney and heart in rats with 5/6 nephrectomy-effects of salt, ARB, DPP4 inhibitor and SGLT2 blocker}, series = {BMC nephrology}, volume = {23}, journal = {BMC nephrology}, number = {1}, publisher = {Springer Nature}, address = {London}, issn = {1471-2369}, doi = {10.1186/s12882-022-02747-1}, pages = {10}, year = {2022}, abstract = {Background Host factors such as angiotensin-converting enzyme 2 (ACE2) and the transmembrane protease, serine-subtype-2 (TMPRSS2) are important factors for SARS-CoV-2 infection. Clinical and pre-clinical studies demonstrated that RAAS-blocking agents can be safely used during a SARS-CoV-2 infection but it is unknown if DPP-4 inhibitors or SGLT2-blockers may promote COVID-19 by increasing the host viral entry enzymes ACE2 and TMPRSS2. Methods We investigated telmisartan, linagliptin and empagliflozin induced effects on renal and cardiac expression of ACE2, TMPRSS2 and key enzymes involved in RAAS (REN, AGTR2, AGT) under high-salt conditions in a non-diabetic experimental 5/6 nephrectomy (5/6 Nx) model. In the present study, the gene expression of Ace2, Tmprss2, Ren, Agtr2 and Agt was assessed with qRT-PCR and the protein expression of ACE2 and TMPRSS2 with immunohistochemistry in the following experimental groups: Sham + normal diet (ND) + placebo (PBO); 5/6Nx + ND + PBO; 5/6Nx + high salt-diet (HSD) + PBO; 5/6Nx + HSD + telmisartan; 5/6Nx + HSD + linagliptin; 5/6Nx + HSD + empagliflozin. Results In the kidney, the expression of Ace2 was not altered on mRNA level under disease and treatment conditions. The renal TMPRSS2 levels (mRNA and protein) were not affected, whereas the cardiac level was significantly increased in 5/6Nx rats. Intriguingly, the elevated TMPRSS2 protein expression in the heart was significantly normalized after treatment with telmisartan, linagliptin and empagliflozin. Conclusions Our study indicated that there is no upregulation regarding host factors potentially promoting SARS-CoV-2 virus entry into host cells when the SGLT2-blocker empagliflozin, telmisartan and the DPP4-inhibitor blocker linagliptin are used. The results obtained in a preclinical, experimental non-diabetic kidney failure model need confirmation in ongoing interventional clinical trials.}, language = {en} } @article{BotteriPeveriBerstadetal.2022, author = {Botteri, Edoardo and Peveri, Giulia and Berstad, Paula and Bagnardi, Vincenzo and Chen, Sairah L. F. and Sandanger, Torkjel M. and Hoff, Geir and Dahm, Christina C. and Antoniussen, Christian S. and Tjonneland, Anne and Eriksen, Anne Kirstine and Skeie, Guri and Perez-Cornago, Aurora and Huerta, Jose Maria and Jakszyn, Paula and Harlid, Sophia and Sundstroem, Bjoern and Barricarte, Aurelio and Monninkhof, Evelyn M. and Derksen, Jeroen W. G. and Schulze, Matthias Bernd and Bueno-de-Mesquita, Bas and Sanchez, Maria-Jose and Cross, Amanda J. and Tsilidis, Konstantinos K. and De Magistris, Maria Santucci and Kaaks, Rudolf and Katzke, Verena and Rothwell, Joseph A. and Laouali, Nasser and Severi, Gianluca and Amiano, Pilar and Contiero, Paolo and Sacerdote, Carlotta and Goldberg, Marcel and Touvier, Mathilde and Freisling, Heinz and Viallon, Vivian and Weiderpass, Elisabete and Riboli, Elio and Gunter, Marc J. and Jenab, Mazda and Ferrari, Pietro}, title = {Changes in lifestyle and risk of colorectal cancer in the European prospective investigation into cancer and nutrition}, series = {The American journal of gastroenterology : AJG}, volume = {118}, journal = {The American journal of gastroenterology : AJG}, number = {4}, publisher = {Lippincott Williams \& Wilkins}, address = {Philadelphia}, issn = {0002-9270}, doi = {10.14309/ajg.0000000000002065}, pages = {702 -- 711}, year = {2022}, abstract = {INTRODUCTION: We investigated the impact of changes in lifestyle habits on colorectal cancer (CRC) risk in a multicountry European cohort. METHODS: We used baseline and follow-up questionnaire data from the European Prospective Investigation into Cancer cohort to assess changes in lifestyle habits and their associations with CRC development. We calculated a healthy lifestyle index (HLI) score based on smoking status, alcohol consumption, body mass index, and physical activity collected at the 2 time points. HLI ranged from 0 (most unfavorable) to 16 (most favorable). We estimated the association between HLI changes and CRC risk using Cox regression models and reported hazard ratios (HR) with 95\% confidence intervals (CI). RESULTS: Among 295,865 participants, 2,799 CRC cases were observed over a median of 7.8 years. The median time between questionnaires was 5.7 years. Each unit increase in HLI from the baseline to the follow-up assessment was associated with a statistically significant 3\% lower CRC risk. Among participants in the top tertile at baseline (HLI > 11), those in the bottom tertile at follow-up (HLI <= 9) had a higher CRC risk (HR 1.34; 95\% CI 1.02-1.75) than those remaining in the top tertile. Among individuals in the bottom tertile at baseline, those in the top tertile at follow-up had a lower risk (HR 0.77; 95\% CI 0.59-1.00) than those remaining in the bottom tertile. DISCUSSION: Improving adherence to a healthy lifestyle was inversely associated with CRC risk, while worsening adherence was positively associated with CRC risk. These results justify and support recommendations for healthy lifestyle changes and healthy lifestyle maintenance for CRC prevention.}, language = {en} } @techreport{BrodeurMikolaCooketal.2024, type = {Working Paper}, author = {Brodeur, Abel and Mikola, Derek and Cook, Nikolai and Brailey, Thomas and Briggs, Ryan and Gendre, Alexandra de and Dupraz, Yannick and Fiala, Lenka and Gabani, Jacopo and Gauriot, Romain and Haddad, Joanne and Lima, Goncalo and Ankel-Peters, J{\"o}rg and Dreber, Anna and Campbell, Douglas and Kattan, Lamis and Fages, Diego Marino and Mierisch, Fabian and Sun, Pu and Wright, Taylor and Connolly, Marie and Hoces de la Guardia, Fernando and Johannesson, Magnus and Miguel, Edward and Vilhuber, Lars and Abarca, Alejandro and Acharya, Mahesh and Adjisse, Sossou Simplice and Akhtar, Ahwaz and Lizardi, Eduardo Alberto Ramirez and Albrecht, Sabina and Andersen, Synve Nygaard and Andlib, Zubaria and Arrora, Falak and Ash, Thomas and Bacher, Etienne and Bachler, Sebastian and Bacon, F{\´e}lix and Bagues, Manuel and Balogh, Timea and Batmanov, Alisher and Barschkett, Mara and Basdil, B. Kaan and Dower, Jaromneda and Castek, Ondrej and Caviglia-Harris, Jill and Strand, Gabriella Chauca and Chen, Shi and Chzhen, Asya and Chung, Jong and Collins, Jason and Coppock, Alexander and Cordeau, Hugo and Couillard, Ben and Crechet, Jonathan and Crippa, Lorenzo and Cui, Jeanne and Czymara, Christian and Daarstad, Haley and Dao, Danh Chi and Dao, Dong and Schmandt, Marco David and Linde, Astrid de and Melo, Lucas De and Deer, Lachlan and Vera, Micole De and Dimitrova, Velichka and Dollbaum, Jan Fabian and Dollbaum, Jan Matti and Donnelly, Michael and Huynh, Luu Duc Toan and Dumbalska, Tsvetomira and Duncan, Jamie and Duong, Kiet Tuan and Duprey, Thibaut and Dworschak, Christoph and Ellingsrud, Sigmund and Elminejad, Ali and Eissa, Yasmine and Erhart, Andrea and Etingin-Frati, Giulian and Fatemi-Pour, Elaheh and Federice, Alexa and Feld, Jan and Fenig, Guidon and Firouzjaeiangalougah, Mojtaba and Fleisje, Erlend and Fortier-Chouinard, Alexandre and Engel, Julia Francesca and Fries, Tilman and Fortier, Reid and Fr{\´e}chet, Nadjim and Galipeau, Thomas and Gallegos, Sebasti{\´a}n and Gangji, Areez and Gao, Xiaoying and Garnache, Clo{\´e} and G{\´a}sp{\´a}r, Attila and Gavrilova, Evelina and Ghosh, Arijit and Gibney, Garreth and Gibson, Grant and Godager, Geir and Goff, Leonard and Gong, Da and Gonz{\´a}lez, Javier and Gretton, Jeremy and Griffa, Cristina and Grigoryeva, Idaliya and Grtting, Maja and Guntermann, Eric and Guo, Jiaqi and Gugushvili, Alexi and Habibnia, Hooman and H{\"a}ffner, Sonja and Hall, Jonathan D. and Hammar, Olle and Kordt, Amund Hanson and Hashimoto, Barry and Hartley, Jonathan S. and Hausladen, Carina I. and Havr{\´a}nek, Tom{\´a}š and Hazen, Jacob and He, Harry and Hepplewhite, Matthew and Herrera-Rodriguez, Mario and Heuer, Felix and Heyes, Anthony and Ho, Anson T. Y. and Holmes, Jonathan and Holzknecht, Armando and Hsu, Yu-Hsiang Dexter and Hu, Shiang-Hung and Huang, Yu-Shiuan and Huebener, Mathias and Huber, Christoph and Huynh, Kim P. and Irsova, Zuzana and Isler, Ozan and Jakobsson, Niklas and Frith, Michael James and Jananji, Rapha{\"e}l and Jayalath, Tharaka A. and Jetter, Michael and John, Jenny and Forshaw, Rachel Joy and Juan, Felipe and Kadriu, Valon and Karim, Sunny and Kelly, Edmund and Dang, Duy Khanh Hoang and Khushboo, Tazia and Kim, Jin and Kjellsson, Gustav and Kjelsrud, Anders and Kotsadam, Andreas and Korpershoek, Jori and Krashinsky, Lewis and Kundu, Suranjana and Kustov, Alexander and Lalayev, Nurlan and Langlois, Audr{\´e}e and Laufer, Jill and Lee-Whiting, Blake and Leibing, Andreas and Lenz, Gabriel and Levin, Joel and Li, Peng and Li, Tongzhe and Lin, Yuchen and Listo, Ariel and Liu, Dan and Lu, Xuewen and Lukmanova, Elvina and Luscombe, Alex and Lusher, Lester R. and Lyu, Ke and Ma, Hai and M{\"a}der, Nicolas and Makate, Clifton and Malmberg, Alice and Maitra, Adit and Mandas, Marco and Marcus, Jan and Margaryan, Shushanik and M{\´a}rk, Lili and Martignano, Andres and Marsh, Abigail and Masetto, Isabella and McCanny, Anthony and McManus, Emma and McWay, Ryan and Metson, Lennard and Kinge, Jonas Minet and Mishra, Sumit and Mohnen, Myra and M{\"o}ller, Jakob and Montambeault, Rosalie and Montpetit, S{\´e}bastien and Morin, Louis-Philippe and Morris, Todd and Moser, Scott and Motoki, Fabio and Muehlenbachs, Lucija and Musulan, Andreea and Musumeci, Marco and Nabin, Munirul and Nchare, Karim and Neubauer, Florian and Nguyen, Quan M. P. and Nguyen, Tuan and Nguyen-Tien, Viet and Niazi, Ali and Nikolaishvili, Giorgi and Nordstrom, Ardyn and N{\"u}, Patrick and Odermatt, Angela and Olson, Matt and ien, Henning and {\"O}lkers, Tim and Vert, Miquel Oliver i. and Oral, Emre and Oswald, Christian and Ousman, Ali and {\"O}zak, {\"O}mer and Pandey, Shubham and Pavlov, Alexandre and Pelli, Martino and Penheiro, Romeo and Park, RyuGyung and Martel, Eva P{\´e}rez and Petrovičov{\´a}, Tereza and Phan, Linh and Prettyman, Alexa and Proch{\´a}zka, Jakub and Putri, Aqila and Quandt, Julian and Qiu, Kangyu and Nguyen, Loan Quynh Thi and Rahman, Andaleeb and Rea, Carson H. and Reiremo, Adam and Ren{\´e}e, La{\"e}titia and Richardson, Joseph and Rivers, Nicholas and Rodrigues, Bruno and Roelofs, William and Roemer, Tobias and Rogeberg, Ole and Rose, Julian and Roskos-Ewoldsen, Andrew and Rosmer, Paul and Sabada, Barbara and Saberian, Soodeh and Salamanca, Nicolas and Sator, Georg and Sawyer, Antoine and Scates, Daniel and Schl{\"u}ter, Elmar and Sells, Cameron and Sen, Sharmi and Sethi, Ritika and Shcherbiak, Anna and Sogaolu, Moyosore and Soosalu, Matt and Srensen, Erik and Sovani, Manali and Spencer, Noah and Staubli, Stefan and Stans, Renske and Stewart, Anya and Stips, Felix and Stockley, Kieran and Strobel, Stephenson and Struby, Ethan and Tang, John and Tanrisever, Idil and Yang, Thomas Tao and Tastan, Ipek and Tatić, Dejan and Tatlow, Benjamin and Seuyong, F{\´e}raud Tchuisseu and Th{\´e}riault, R{\´e}mi and Thivierge, Vincent and Tian, Wenjie and Toma, Filip-Mihai and Totarelli, Maddalena and Tran, Van-Anh and Truong, Hung and Tsoy, Nikita and Tuzcuoglu, Kerem and Ubfal, Diego and Villalobos, Laura and Walterskirchen, Julian and Wang, Joseph Taoyi and Wattal, Vasudha and Webb, Matthew D. and Weber, Bryan and Weisser, Reinhard and Weng, Wei-Chien and Westheide, Christian and White, Kimberly and Winter, Jacob and Wochner, Timo and Woerman, Matt and Wong, Jared and Woodard, Ritchie and Wroński, Marcin and Yazbeck, Myra and Yang, Gustav Chung and Yap, Luther and Yassin, Kareman and Ye, Hao and Yoon, Jin Young and Yurris, Chris and Zahra, Tahreen and Zaneva, Mirela and Zayat, Aline and Zhang, Jonathan and Zhao, Ziwei and Yaolang, Zhong}, title = {Mass reproducibility and replicability}, series = {I4R discussion paper series}, journal = {I4R discussion paper series}, number = {107}, publisher = {Institute for Replication}, address = {Essen}, issn = {2752-1931}, pages = {250}, year = {2024}, abstract = {This study pushes our understanding of research reliability by reproducing and replicating claims from 110 papers in leading economic and political science journals. The analysis involves computational reproducibility checks and robustness assessments. It reveals several patterns. First, we uncover a high rate of fully computationally reproducible results (over 85\%). Second, excluding minor issues like missing packages or broken pathways, we uncover coding errors for about 25\% of studies, with some studies containing multiple errors. Third, we test the robustness of the results to 5,511 re-analyses. We find a robustness reproducibility of about 70\%. Robustness reproducibility rates are relatively higher for re-analyses that introduce new data and lower for re-analyses that change the sample or the definition of the dependent variable. Fourth, 52\% of re-analysis effect size estimates are smaller than the original published estimates and the average statistical significance of a re-analysis is 77\% of the original. Lastly, we rely on six teams of researchers working independently to answer eight additional research questions on the determinants of robustness reproducibility. Most teams find a negative relationship between replicators' experience and reproducibility, while finding no relationship between reproducibility and the provision of intermediate or even raw data combined with the necessary cleaning codes.}, language = {en} }