@misc{YangDarkoHuangetal.2017,
  author    = {Yang, Xiaoping and Darko, Kwame Oteng and Huang, Yanjun and He, Caimei and Yang, Huansheng and He, Shanping and Li, Jianzhong and Li, Jian and Hocher, Berthold and Yin, Yulong},
  title     = {Resistant starch regulates gut microbiota},
  series = {Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry and pharmacology},
  volume    = {42},
  journal   = {Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry and pharmacology},
  number    = {1},
  publisher = {Karger},
  address   = {Basel},
  issn      = {1015-8987},
  doi       = {10.1159/000477386},
  pages     = {306 -- 318},
  year      = {2017},
  abstract  = {Starch is one of the most popular nutritional sources for both human and animals. Due to the variation of its nutritional traits and biochemical specificities, starch has been classified into rapidly digestible, slowly digestible and resistant starch. Resistant starch has its own unique chemical structure, and various forms of resistant starch are commercially available. It has been found being a multiple-functional regulator for treating metabolic dysfunction. Different functions of resistant starch such as modulation of the gut microbiota, gut peptides, circulating growth factors, circulating inflammatory mediators have been characterized by animal studies and clinical trials. In this mini-review, recent remarkable progress in resistant starch on gut microbiota, particularly the effect of structure, biochemistry and cell signaling on nutrition has been summarized, with highlights on its regulatory effect on gut microbiota.},
  language  = {en}
}
@article{TaoSuXuetal.2018,
  author    = {Tao, Ting and Su, Qiongli and Xu, Simeng and Deng, Jun and Zhou, Sichun and Zhuang, Yu and Huang, Yanjun and He, Caimei and He, Shanping and Peng, Mei and Hocher, Berthold and Yang, Xiaoping},
  title     = {Down-regulation of PKM2 decreases FASN expression in bladder cancer cells through AKT/mTOR/SREBP-1c axis},
  series = {Journal of cellular physiology},
  volume    = {234},
  journal   = {Journal of cellular physiology},
  number    = {3},
  publisher = {Wiley},
  address   = {Hoboken},
  issn      = {0021-9541},
  doi       = {10.1002/jcp.27129},
  pages     = {3088 -- 3104},
  year      = {2018},
  abstract  = {Fatty acid synthase (FASN) catalyzing the terminal steps in the de novo biogenesis of fatty acids is correlated with low survival and high disease recurrence in patients with bladder cancer. Pyruvate kinase M2 (PKM2) regulates the final step of glycolysis levels and provides a growth advantage to tumors. However, it is unclear whether the change of PKM2 has an effect on FASN and what is the mechanisms underlying. Here we describe a novel function of PKM2 in control of lipid metabolism by mediating transcriptional activation of FASN, showing the reduced expression of sterol regulatory element binding protein 1c (SREBP-1c). We first discovered that PKM2 physically interacts with the SREBP-1c using biochemical approaches, and downregulation of PKM2 reduced the expression of SREBP-1c by inactivating the AKT/mTOR signaling pathway, which in turn directly suppressed the transcription of major lipogenic genes FASN to reduce tumor growths. Furthermore, either PKM2 inhibitor-Shikonin or FASN inhibitor-TVB-3166 alone induced a strong antiproliferative and anticolony forming effect in bladder cancer cell line. The combination of both inhibitors exhibits a super synergistic effect on blocking the bladder cancer cells growth. It provides a new target and scientific basis for the treatment of bladder cancer.},
  language  = {en}
}
@article{HeHuangLietal.2018,
  author    = {He, Yongli and Huang, Jianping and Li, Dongdong and Xie, Yongkun and Zhang, Guolong and Qi, Yulei and Wang, Shanshan and Totz, Sonja Juliana},
  title     = {Comparison of the effect of land-sea thermal contrast on interdecadal variations in winter and summer blockings},
  series = {Climate dynamics : observational, theoretical and computational research on the climate system},
  volume    = {51},
  journal   = {Climate dynamics : observational, theoretical and computational research on the climate system},
  number    = {4},
  publisher = {Springer},
  address   = {New York},
  issn      = {0930-7575},
  doi       = {10.1007/s00382-017-3954-9},
  pages     = {1275 -- 1294},
  year      = {2018},
  abstract  = {The influence of winter and summer land-sea surface thermal contrast on blocking for 1948-2013 is investigated using observations and the coupled model intercomparison project outputs. The land-sea index (LSI) is defined to measure the changes of zonal asymmetric thermal forcing under global warming. The summer LSI shows a slower increasing trend than winter during this period. For the positive of summer LSI, the EP flux convergence induced by the land-sea thermal forcing in the high latitude becomes weaker than normal, which induces positive anomaly of zonal-mean westerly and double-jet structure. Based on the quasiresonance amplification mechanism, the narrow and reduced westerly tunnel between two jet centers provides a favor environment for more frequent blocking. Composite analysis demonstrates that summer blocking shows an increasing trend of event numbers and a decreasing trend of durations. The numbers of the short-lived blocking persisting for 5-9 days significantly increases and the numbers of the long-lived blocking persisting for longer than 10 days has a weak increase than that in negative phase of summer LSI. The increasing transient wave activities induced by summer LSI is responsible for the decreasing duration of blockings. The increasing blocking due to summer LSI can further strengthen the continent warming and increase the summer LSI, which forms a positive feedback. The opposite dynamical effect of LSI on summer and winter blocking are discussed and found that the LSI-blocking negative feedback partially reduces the influence of the above positive feedback and induce the weak summer warming rate.},
  language  = {en}
}
@article{HeLiuLuetal.2017,
  author    = {He, Jing and Liu, Zhi-Wei and Lu, Yong-Ping and Li, Tao-Yuan and Liang, Xu-Jing and Arck, Petra and Huang, Si-Min and Hocher, Berthold and Chen, You-Peng},
  title     = {A systematic review and meta-analysis of influenza a virus infection during pregnancy associated with an increased risk for stillbirth and low birth weight},
  series = {Kidney \& blood pressure research : official organ of the Gesellschaft f{\"u}r Nephrologie ; official organ of the Deutsche Liga zur Bek{\"a}mpfung des Hohen Blutdruckes e.V., Deutsche Hypertonie-Gesellschaft},
  volume    = {42},
  journal   = {Kidney \& blood pressure research : official organ of the Gesellschaft f{\"u}r Nephrologie ; official organ of the Deutsche Liga zur Bek{\"a}mpfung des Hohen Blutdruckes e.V., Deutsche Hypertonie-Gesellschaft},
  number    = {2},
  publisher = {Karger},
  address   = {Basel},
  issn      = {1420-4096},
  doi       = {10.1159/000477221},
  pages     = {232 -- 243},
  year      = {2017},
  abstract  = {Background/Aims: Impaired pregnancy outcomes, such as low birth weight are associated with increased disease risk in later life, however little is known about the impact of common infectious diseases during pregnancy on birth weight. The study had two aims: a) to investigate risk factors of influenza virus infection during pregnancy, and b) to analyze the impact of influenza virus infection on pregnancy outcome, especially birth weight. Methods: Prospective and retrospective observational studies found in PubMed, MEDLINE, Embase, Google Scholar, and WangFang database were included in this meta analysis. Data of included studies was extracted and analyzed by the RevMan software. Results: Pregnant women with anemia (P=0.004, RR=1.46, 95\% CI: 1.13-1.88), obesity (P<0.00001, RR=1.35, 95\% CI: 1.25-1.46) and asthma (P<0.00001, RR=1.99, 95\% CI: 1.67-2.37) had higher rates of influenza virus infection. Regarding birth outcomes, influenza A virus infection did not affect the likelihood for cesarean section. Mothers with influenza had a higher rate of stillbirth (P=0.04, RR=2.36, 95\% CI: 1.05-5.31), and their offspring had low 5-minute APGR Scores (P=0.009, RR=1.39, 95\% CI: 1.08-1.79). Furthermore, the rate for birth weight < 2500g (P=0.04, RR=1.71, 95\% CI: 1.03-2.84) was increased. Conclusion: Results of this study showed that anemia, asthma and obesity during pregnancy are risk factors influenza A virus infection during pregnancy. Moreover, gestational influenza A infection impairs pregnancy outcomes and increases the risk for low birth weight, a known risk factor for later life disease susceptibility.},
  language  = {en}
}
@article{SunHuangMengetal.2012,
  author    = {Sun, Sheng-Yun and Huang, Jin and Meng, Min-Jie and Lu, Jia-Hai and Hocher, Berthold and Liu, Kang-Li and Yang, Qin-He and Zhu, Xiao-Feng},
  title     = {Improvement of lipid profile and reduction of body weight by Shan He Jian Fei Granules in high fat diet-induced obese rats},
  series = {Clinical laboratory : the peer reviewed journal for clinical laboratories and laboratories related to blood transfusion},
  volume    = {58},
  journal   = {Clinical laboratory : the peer reviewed journal for clinical laboratories and laboratories related to blood transfusion},
  number    = {1-2},
  publisher = {Clin Lab Publ., Verl. Klinisches Labor},
  address   = {Heidelberg},
  issn      = {1433-6510},
  pages     = {81 -- 87},
  year      = {2012},
  abstract  = {Background: The goal was to study lipid profiles (TG, TC, LDL, HDL), effects on serum leptin, and fat tissue adiponectin, and resistin as well as body weight effects of Shan He Jian Fei Granules (SHJFG) in rats on a high fat diet. Methods: Rats were randomly divided into five groups: normal control group fed with normal fat diet, rats on high fat diet receiving low dosage, middle dosage, high dosage of Shan He Jian Fei Granules (SHJFG) as well as a high fat diet group receiving placebo. Rats were treated for 8 weeks. Body weight and naso-anal length of each rat were recorded and Lee's index was calculated. Serum TG, TC, LDL, HDL and leptin concentrations were analyzed. The gene expressions of adiponectin and resistin in adipose tissues were tested by RT-PCR. Results: Compared to the high-fat diet group, body weights, Lee's indexes, weight of fat tissues and serum TG, TC, LDL and leptin of SHJFG groups significantly decreased (p<0.05), whereas mRNA expressions of adiponectin and resistin of SHJFG groups significantly increased (p<0.05). Conclusions: SHJFG could significantly lower body weight and serum TG, TC, and LDL of obese rats. The effects of SHJFG in lowering leptin synthesis and raising mRNA expression of adiponectin and resistin in fat tissues may act as part of the mechanisms in lowering body weight of obese rats. Further studies are needed to demonstrate whether SHJFG may also reduce overall cardiovascular morbidity and mortality like other lipid lowering drugs.},
  language  = {en}
}
@article{WuttkeLiLietal.2019,
  author    = {Wuttke, Matthias and Li, Yong and Li, Man and Sieber, Karsten B. and Feitosa, Mary F. and Gorski, Mathias and Tin, Adrienne and Wang, Lihua and Chu, Audrey Y. and Hoppmann, Anselm and Kirsten, Holger and Giri, Ayush and Chai, Jin-Fang and Sveinbjornsson, Gardar and Tayo, Bamidele O. and Nutile, Teresa and Fuchsberger, Christian and Marten, Jonathan and Cocca, Massimiliano and Ghasemi, Sahar and Xu, Yizhe and Horn, Katrin and Noce, Damia and Van der Most, Peter J. and Sedaghat, Sanaz and Yu, Zhi and Akiyama, Masato and Afaq, Saima and Ahluwalia, Tarunveer Singh and Almgren, Peter and Amin, Najaf and Arnlov, Johan and Bakker, Stephan J. L. and Bansal, Nisha and Baptista, Daniela and Bergmann, Sven and Biggs, Mary L. and Biino, Ginevra and Boehnke, Michael and Boerwinkle, Eric and Boissel, Mathilde and B{\"o}ttinger, Erwin and Boutin, Thibaud S. and Brenner, Hermann and Brumat, Marco and Burkhardt, Ralph and Butterworth, Adam S. and Campana, Eric and Campbell, Archie and Campbell, Harry and Canouil, Mickael and Carroll, Robert J. and Catamo, Eulalia and Chambers, John C. and Chee, Miao-Ling and Chee, Miao-Li and Chen, Xu and Cheng, Ching-Yu and Cheng, Yurong and Christensen, Kaare and Cifkova, Renata and Ciullo, Marina and Concas, Maria Pina and Cook, James P. and Coresh, Josef and Corre, Tanguy and Sala, Cinzia Felicita and Cusi, Daniele and Danesh, John and Daw, E. Warwick and De Borst, Martin H. and De Grandi, Alessandro and De Mutsert, Renee and De Vries, Aiko P. J. and Degenhardt, Frauke and Delgado, Graciela and Demirkan, Ayse and Di Angelantonio, Emanuele and Dittrich, Katalin and Divers, Jasmin and Dorajoo, Rajkumar and Eckardt, Kai-Uwe and Ehret, Georg and Elliott, Paul and Endlich, Karlhans and Evans, Michele K. and Felix, Janine F. and Foo, Valencia Hui Xian and Franco, Oscar H. and Franke, Andre and Freedman, Barry I. and Freitag-Wolf, Sandra and Friedlander, Yechiel and Froguel, Philippe and Gansevoort, Ron T. and Gao, He and Gasparini, Paolo and Gaziano, J. Michael and Giedraitis, Vilmantas and Gieger, Christian and Girotto, Giorgia and Giulianini, Franco and Gogele, Martin and Gordon, Scott D. and Gudbjartsson, Daniel F. and Gudnason, Vilmundur and Haller, Toomas and Hamet, Pavel and Harris, Tamara B. and Hartman, Catharina A. and Hayward, Caroline and Hellwege, Jacklyn N. and Heng, Chew-Kiat and Hicks, Andrew A. and Hofer, Edith and Huang, Wei and Hutri-Kahonen, Nina and Hwang, Shih-Jen and Ikram, M. Arfan and Indridason, Olafur S. and Ingelsson, Erik and Ising, Marcus and Jaddoe, Vincent W. V. and Jakobsdottir, Johanna and Jonas, Jost B. and Joshi, Peter K. and Josyula, Navya Shilpa and Jung, Bettina and Kahonen, Mika and Kamatani, Yoichiro and Kammerer, Candace M. and Kanai, Masahiro and Kastarinen, Mika and Kerr, Shona M. and Khor, Chiea-Chuen and Kiess, Wieland and Kleber, Marcus E. and Koenig, Wolfgang and Kooner, Jaspal S. and Korner, Antje and Kovacs, Peter and Kraja, Aldi T. and Krajcoviechova, Alena and Kramer, Holly and Kramer, Bernhard K. and Kronenberg, Florian and Kubo, Michiaki and Kuhnel, Brigitte and Kuokkanen, Mikko and Kuusisto, Johanna and La Bianca, Martina and Laakso, Markku and Lange, Leslie A. and Langefeld, Carl D. and Lee, Jeannette Jen-Mai and Lehne, Benjamin and Lehtimaki, Terho and Lieb, Wolfgang and Lim, Su-Chi and Lind, Lars and Lindgren, Cecilia M. and Liu, Jun and Liu, Jianjun and Loeffler, Markus and Loos, Ruth J. F. and Lucae, Susanne and Lukas, Mary Ann and Lyytikainen, Leo-Pekka and Magi, Reedik and Magnusson, Patrik K. E. and Mahajan, Anubha and Martin, Nicholas G. and Martins, Jade and Marz, Winfried and Mascalzoni, Deborah and Matsuda, Koichi and Meisinger, Christa and Meitinger, Thomas and Melander, Olle and Metspalu, Andres and Mikaelsdottir, Evgenia K. and Milaneschi, Yuri and Miliku, Kozeta and Mishra, Pashupati P. and Program, V. A. Million Veteran and Mohlke, Karen L. and Mononen, Nina and Montgomery, Grant W. and Mook-Kanamori, Dennis O. and Mychaleckyj, Josyf C. and Nadkarni, Girish N. and Nalls, Mike A. and Nauck, Matthias and Nikus, Kjell and Ning, Boting and Nolte, Ilja M. and Noordam, Raymond and Olafsson, Isleifur and Oldehinkel, Albertine J. and Orho-Melander, Marju and Ouwehand, Willem H. and Padmanabhan, Sandosh and Palmer, Nicholette D. and Palsson, Runolfur and Penninx, Brenda W. J. H. and Perls, Thomas and Perola, Markus and Pirastu, Mario and Pirastu, Nicola and Pistis, Giorgio and Podgornaia, Anna I. and Polasek, Ozren and Ponte, Belen and Porteous, David J. and Poulain, Tanja and Pramstaller, Peter P. and Preuss, Michael H. and Prins, Bram P. and Province, Michael A. and Rabelink, Ton J. and Raffield, Laura M. and Raitakari, Olli T. and Reilly, Dermot F. and Rettig, Rainer and Rheinberger, Myriam and Rice, Kenneth M. and Ridker, Paul M. and Rivadeneira, Fernando and Rizzi, Federica and Roberts, David J. and Robino, Antonietta and Rossing, Peter and Rudan, Igor and Rueedi, Rico and Ruggiero, Daniela and Ryan, Kathleen A. and Saba, Yasaman and Sabanayagam, Charumathi and Salomaa, Veikko and Salvi, Erika and Saum, Kai-Uwe and Schmidt, Helena and Schmidt, Reinhold and Ben Schottker, and Schulz, Christina-Alexandra and Schupf, Nicole and Shaffer, Christian M. and Shi, Yuan and Smith, Albert V. and Smith, Blair H. and Soranzo, Nicole and Spracklen, Cassandra N. and Strauch, Konstantin and Stringham, Heather M. and Stumvoll, Michael and Svensson, Per O. and Szymczak, Silke and Tai, E-Shyong and Tajuddin, Salman M. and Tan, Nicholas Y. Q. and Taylor, Kent D. and Teren, Andrej and Tham, Yih-Chung and Thiery, Joachim and Thio, Chris H. L. and Thomsen, Hauke and Thorleifsson, Gudmar and Toniolo, Daniela and Tonjes, Anke and Tremblay, Johanne and Tzoulaki, Ioanna and Uitterlinden, Andre G. and Vaccargiu, Simona and Van Dam, Rob M. and Van der Harst, Pim and Van Duijn, Cornelia M. and Edward, Digna R. Velez and Verweij, Niek and Vogelezang, Suzanne and Volker, Uwe and Vollenweider, Peter and Waeber, Gerard and Waldenberger, Melanie and Wallentin, Lars and Wang, Ya Xing and Wang, Chaolong and Waterworth, Dawn M. and Bin Wei, Wen and White, Harvey and Whitfield, John B. and Wild, Sarah H. and Wilson, James F. and Wojczynski, Mary K. and Wong, Charlene and Wong, Tien-Yin and Xu, Liang and Yang, Qiong and Yasuda, Masayuki and Yerges-Armstrong, Laura M. and Zhang, Weihua and Zonderman, Alan B. and Rotter, Jerome I. and Bochud, Murielle and Psaty, Bruce M. and Vitart, Veronique and Wilson, James G. and Dehghan, Abbas and Parsa, Afshin and Chasman, Daniel I. and Ho, Kevin and Morris, Andrew P. and Devuyst, Olivier and Akilesh, Shreeram and Pendergrass, Sarah A. and Sim, Xueling and Boger, Carsten A. and Okada, Yukinori and Edwards, Todd L. and Snieder, Harold and Stefansson, Kari and Hung, Adriana M. and Heid, Iris M. and Scholz, Markus and Teumer, Alexander and Kottgen, Anna and Pattaro, Cristian},
  title     = {A catalog of genetic loci associated with kidney function from analyses of a million individuals},
  series = {Nature genetics},
  volume    = {51},
  journal   = {Nature genetics},
  number    = {6},
  publisher = {Nature Publ. Group},
  address   = {New York},
  organization    = {Lifelines COHort Study},
  issn      = {1061-4036},
  doi       = {10.1038/s41588-019-0407-x},
  pages     = {957 -- +},
  year      = {2019},
  abstract  = {Chronic kidney disease (CKD) is responsible for a public health burden with multi-systemic complications. Through transancestry meta-analysis of genome-wide association studies of estimated glomerular filtration rate (eGFR) and independent replication (n = 1,046,070), we identified 264 associated loci (166 new). Of these,147 were likely to be relevant for kidney function on the basis of associations with the alternative kidney function marker blood urea nitrogen (n = 416,178). Pathway and enrichment analyses, including mouse models with renal phenotypes, support the kidney as the main target organ. A genetic risk score for lower eGFR was associated with clinically diagnosed CKD in 452,264 independent individuals. Colocalization analyses of associations with eGFR among 783,978 European-ancestry individuals and gene expression across 46 human tissues, including tubulo-interstitial and glomerular kidney compartments, identified 17 genes differentially expressed in kidney. Fine-mapping highlighted missense driver variants in 11 genes and kidney-specific regulatory variants. These results provide a comprehensive priority list of molecular targets for translational research.},
  language  = {en}
}
@article{HuangQiaoXuetal.2021,
  author    = {Huang, Lixing and Qiao, Ying and Xu, Wei and Gong, Linfeng and He, Rongchao and Qi, Weilu and Gao, Qiancheng and Cai, Hongyan and Grossart, Hans-Peter and Yan, Qingpi},
  title     = {Full-length transcriptome},
  series = {Frontiers in immunology},
  volume    = {12},
  journal   = {Frontiers in immunology},
  publisher = {Frontiers Media},
  address   = {Lausanne},
  issn      = {1664-3224},
  doi       = {10.3389/fimmu.2021.737332},
  pages     = {18},
  year      = {2021},
  abstract  = {Fish is considered as a supreme model for clarifying the evolution and regulatory mechanism of vertebrate immunity. However, the knowledge of distinct immune cell populations in fish is still limited, and further development of techniques advancing the identification of fish immune cell populations and their functions are required. Single cell RNA-seq (scRNA-seq) has provided a new approach for effective in-depth identification and characterization of cell subpopulations. Current approaches for scRNA-seq data analysis usually rely on comparison with a reference genome and hence are not suited for samples without any reference genome, which is currently very common in fish research. Here, we present an alternative, i.e. scRNA-seq data analysis with a full-length transcriptome as a reference, and evaluate this approach on samples from Epinephelus coioides-a teleost without any published genome. We show that it reconstructs well most of the present transcripts in the scRNA-seq data achieving a sensitivity equivalent to approaches relying on genome alignments of related species. Based on cell heterogeneity and known markers, we characterized four cell types: T cells, B cells, monocytes/macrophages (Mo/M phi) and NCC (non-specific cytotoxic cells). Further analysis indicated the presence of two subsets of Mo/M phi including M1 and M2 type, as well as four subsets in B cells, i.e. mature B cells, immature B cells, pre B cells and early-pre B cells. Our research will provide new clues for understanding biological characteristics, development and function of immune cell populations of teleost. Furthermore, our approach provides a reliable alternative for scRNA-seq data analysis in teleost for which no reference genome is currently available.},
  language  = {en}
}
@article{CaoNiSummersetal.2019,
  author    = {Cao, Xing and Ni, Binbin and Summers, Danny and Shprits, Yuri and Gu, Xudong and Fu, Song and Lou, Yuequn and Zhang, Yang and Ma, Xin and Zhang, Wenxun and Huang, He and Yi, Juan},
  title     = {Sensitivity of EMIC wave-driven scattering loss of ring current protons to wave normal angle distribution},
  series = {Geophysical research letters},
  volume    = {46},
  journal   = {Geophysical research letters},
  number    = {2},
  publisher = {American Geophysical Union},
  address   = {Washington},
  issn      = {0094-8276},
  doi       = {10.1029/2018GL081550},
  pages     = {590 -- 598},
  year      = {2019},
  abstract  = {Electromagnetic ion cyclotron waves have long been recognized to play a crucial role in the dynamic loss of ring current protons. While the field-aligned propagation approximation of electromagnetic ion cyclotron waves was widely used to quantify the scattering loss of ring current protons, in this study, we find that the wave normal distribution strongly affects the pitch angle scattering efficiency of protons. Increase of peak normal angle or angular width can considerably reduce the scattering rates of <= 10 keV protons. For >10 keV protons, the field-aligned propagation approximation results in a pronounced underestimate of the scattering of intermediate equatorial pitch angle protons and overestimates the scattering of high equatorial pitch angle protons by orders of magnitude. Our results suggest that the wave normal distribution of electromagnetic ion cyclotron waves plays an important role in the pitch angle evolution and scattering loss of ring current protons and should be incorporated in future global modeling of ring current dynamics.},
  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}
}