@article{WarringtonBeaumontHorikoshietal.2019, author = {Warrington, Nicole and Beaumont, Robin and Horikoshi, Momoko and Day, Felix R. and Helgeland, {\O}yvind and Laurin, Charles and Bacelis, Jonas and Peng, Shouneng and Hao, Ke and Feenstra, Bjarke and Wood, Andrew R. and Mahajan, Anubha and Tyrrell, Jessica and Robertson, Neil R. and Rayner, N. William and Qiao, Zhen and Moen, Gunn-Helen and Vaudel, Marc and Marsit, Carmen and Chen, Jia and Nodzenski, Michael and Schnurr, Theresia M. and Zafarmand, Mohammad Hadi and Bradfield, Jonathan P. and Grarup, Niels and Kooijman, Marjolein N. and Li-Gao, Ruifang and Geller, Frank and Ahluwalia, Tarunveer Singh and Paternoster, Lavinia and Rueedi, Rico and Huikari, Ville and Hottenga, Jouke-Jan and Lyytik{\"a}inen, Leo-Pekka and Cavadino, Alana and Metrustry, Sarah and Cousminer, Diana L. and Wu, Ying and Thiering, Elisabeth Paula and Wang, Carol A. and Have, Christian Theil and Vilor-Tejedor, Natalia and Joshi, Peter K. and Painter, Jodie N. and Ntalla, Ioanna and Myhre, Ronny and Pitk{\"a}nen, Niina and van Leeuwen, Elisabeth M. and Joro, Raimo and Lagou, Vasiliki and Richmond, Rebecca C. and Espinosa, Ana and Barton, Sheila J. and Inskip, Hazel M. and Holloway, John W. and Santa-Marina, Loreto and Estivill, Xavier and Ang, Wei and Marsh, Julie A. and Reichetzeder, Christoph and Marullo, Letizia and Hocher, Berthold and Lunetta, Kathryn L. and Murabito, Joanne M. and Relton, Caroline L. and Kogevinas, Manolis and Chatzi, Leda and Allard, Catherine and Bouchard, Luigi and Hivert, Marie-France and Zhang, Ge and Muglia, Louis J. and Heikkinen, Jani and Morgen, Camilla S. and van Kampen, Antoine H. C. and van Schaik, Barbera D. C. and Mentch, Frank D. and Langenberg, Claudia and Scott, Robert A. and Zhao, Jing Hua and Hemani, Gibran and Ring, Susan M. and Bennett, Amanda J. and Gaulton, Kyle J. and Fernandez-Tajes, Juan and van Zuydam, Natalie R. and Medina-Gomez, Carolina and de Haan, Hugoline G. and Rosendaal, Frits R. and Kutalik, Zolt{\´a}n and Marques-Vidal, Pedro and Das, Shikta and Willemsen, Gonneke and Mbarek, Hamdi and M{\"u}ller-Nurasyid, Martina and Standl, Marie and Appel, Emil V. R. and Fonvig, Cilius Esmann and Trier, Caecilie and van Beijsterveldt, Catharina E. M. and Murcia, Mario and Bustamante, Mariona and Bon{\`a}s-Guarch, S{\´i}lvia and Hougaard, David M. and Mercader, Josep M. and Linneberg, Allan and Schraut, Katharina E. and Lind, Penelope A. and Medland, Sarah Elizabeth and Shields, Beverley M. and Knight, Bridget A. and Chai, Jin-Fang and Panoutsopoulou, Kalliope and Bartels, Meike and S{\´a}nchez, Friman and Stokholm, Jakob and Torrents, David and Vinding, Rebecca K. and Willems, Sara M. and Atalay, Mustafa and Chawes, Bo L. and Kovacs, Peter and Prokopenko, Inga and Tuke, Marcus A. and Yaghootkar, Hanieh and Ruth, Katherine S. and Jones, Samuel E. and Loh, Po-Ru and Murray, Anna and Weedon, Michael N. and T{\"o}njes, Anke and Stumvoll, Michael and Michaelsen, Kim Fleischer and Eloranta, Aino-Maija and Lakka, Timo A. and van Duijn, Cornelia M. and Kiess, Wieland and Koerner, Antje and Niinikoski, Harri and Pahkala, Katja and Raitakari, Olli T. and Jacobsson, Bo and Zeggini, Eleftheria and Dedoussis, George V. and Teo, Yik-Ying and Saw, Seang-Mei and Montgomery, Grant W. and Campbell, Harry and Wilson, James F. and Vrijkotte, Tanja G. M. and Vrijheid, Martine and de Geus, Eco J. C. N. and Hayes, M. Geoffrey and Kadarmideen, Haja N. and Holm, Jens-Christian and Beilin, Lawrence J. and Pennell, Craig E. and Heinrich, Joachim and Adair, Linda S. and Borja, Judith B. and Mohlke, Karen L. and Eriksson, Johan G. and Widen, Elisabeth E. and Hattersley, Andrew T. and Spector, Tim D. and Kaehoenen, Mika and Viikari, Jorma S. and Lehtimaeki, Terho and Boomsma, Dorret I. and Sebert, Sylvain and Vollenweider, Peter and Sorensen, Thorkild I. A. and Bisgaard, Hans and Bonnelykke, Klaus and Murray, Jeffrey C. and Melbye, Mads and Nohr, Ellen A. and Mook-Kanamori, Dennis O. and Rivadeneira, Fernando and Hofman, Albert and Felix, Janine F. and Jaddoe, Vincent W. V. and Hansen, Torben and Pisinger, Charlotta and Vaag, Allan A. and Pedersen, Oluf and Uitterlinden, Andre G. and Jarvelin, Marjo-Riitta and Power, Christine and Hypponen, Elina and Scholtens, Denise M. and Lowe, William L. and Smith, George Davey and Timpson, Nicholas J. and Morris, Andrew P. and Wareham, Nicholas J. and Hakonarson, Hakon and Grant, Struan F. A. and Frayling, Timothy M. and Lawlor, Debbie A. and Njolstad, Pal R. and Johansson, Stefan and Ong, Ken K. and McCarthy, Mark I. and Perry, John R. B. and Evans, David M. and Freathy, Rachel M.}, title = {Maternal and fetal genetic effects on birth weight and their relevance to cardio-metabolic risk factors}, series = {Nature genetics}, volume = {51}, journal = {Nature genetics}, number = {5}, publisher = {Nature Publ. Group}, address = {New York}, organization = {EGG Consortium}, issn = {1061-4036}, pages = {804 -- +}, year = {2019}, abstract = {Birth weight variation is influenced by fetal and maternal genetic and non-genetic factors, and has been reproducibly associated with future cardio-metabolic health outcomes. In expanded genome-wide association analyses of own birth weight (n = 321,223) and offspring birth weight (n = 230,069 mothers), we identified 190 independent association signals (129 of which are novel). We used structural equation modeling to decompose the contributions of direct fetal and indirect maternal genetic effects, then applied Mendelian randomization to illuminate causal pathways. For example, both indirect maternal and direct fetal genetic effects drive the observational relationship between lower birth weight and higher later blood pressure: maternal blood pressure-raising alleles reduce offspring birth weight, but only direct fetal effects of these alleles, once inherited, increase later offspring blood pressure. Using maternal birth weight-lowering genotypes to proxy for an adverse intrauterine environment provided no evidence that it causally raises offspring blood pressure, indicating that the inverse birth weight-blood pressure association is attributable to genetic effects, and not to intrauterine programming.}, language = {en} } @article{LiLuTsuprykovetal.2018, author = {Li, Jian and Lu, Yong-Ping and Tsuprykov, Oleg and Hasan, Ahmed Abdallah Abdalrahman Mohamed and Reichetzeder, Christoph and Tian, Mei and Zhang, Xiao Li and Zhang, Qin and Sun, Guo-Ying and Guo, Jingli and Gaballa, Mohamed Mahmoud Salem Ahmed and Peng, Xiao-Ning and Lin, Ge and Hocher, Berthold}, title = {Folate treatment of pregnant rat dams abolishes metabolic effects in female offspring induced by a paternal pre-conception unhealthy diet}, series = {Diabetologia : journal of the European Association for the Study of Diabetes (EASD)}, volume = {61}, journal = {Diabetologia : journal of the European Association for the Study of Diabetes (EASD)}, number = {8}, publisher = {Springer}, address = {New York}, issn = {0012-186X}, doi = {10.1007/s00125-018-4635-x}, pages = {1862 -- 1876}, year = {2018}, abstract = {Aims/hypothesis Paternal high-fat diet prior to mating programmes impaired glucose tolerance in female offspring. We examined whether the metabolic consequences in offspring could be abolished by folate treatment of either the male rats before mating or the corresponding female rats during pregnancy. Methods Male F0 rats were fed either control diet or high-fat, high-sucrose and high-salt diet (HFSSD), with or without folate, before mating. Male rats were mated with control-diet-fed dams. After mating, the F0 dams were fed control diet with or without folate during pregnancy.}, language = {en} } @article{ZhangNajmanMeietal.2019, author = {Zhang, Peng and Najman, Yani and Mei, Lianfu and Millar, Ian and Sobel, Edward and Carter, Andrew and Barfod, Dan and Dhuime, Bruno and Garzanti, Eduardo and Govin, Gwladys and Vezzoli, Giovanni and Hu, Xiaolin}, title = {Palaeodrainage evolution of the large rivers of East Asia, and Himalayan-Tibet tectonics}, series = {Earth science reviews}, volume = {192}, journal = {Earth science reviews}, publisher = {Elsevier}, address = {Amsterdam}, issn = {0012-8252}, doi = {10.1016/j.earscirev.2019.02.003}, pages = {601 -- 630}, year = {2019}, abstract = {A number of sedimentary provenance studies have been undertaken in order to determine whether the palaeo-Red River was once a river of continental proportions into which the upper reaches of the Yangtze, Salween, Mekong, Irrawaddy, and Yarlung drained. We have assessed the evidence that the Yarlung originally flowed into the palaeo-Red river, and then sequentially into the Irrawaddy and Brahmaputra, connecting to the latter first via the Lohit and then the Siang. For this river system, we have integrated our new data from the Paleogene-Recent Irrawaddy drainage basin (detrital zircon U-Pb with Hf and fission track, rutile U-Pb, mica Ar-Ar, bulk rock Sr-Nd, and petrography) with previously published data, to produce a palaeodrainage model that is consistent with all datasets. In our model, the Yarlung never flowed into the Irrawaddy drainage: during the Paleogene, the Yarlung suture zone was an internally drained basin, and from Neogene times onwards the Yarlung drained into the Brahmaputra in the Bengal Basin. The Central Myanmar Basin, through which the Irrawaddy River flows today, received predominantly locally-derived detritus until the Middle Eocene, the Irrawaddy initiated as a through-going river draining the Mogok Metamorphic Belt and Bomi-Chayu granites to the north sometime in the Late Eocene to Early Oligocene, and the river was dominated by a stable MMB-dominated drainage throughout the Neogene to present day. Existing evidence does not support any connection between the Yarlung and the Red River in the past, but there is a paucity of suitable palaeo-Red River deposits with which to make a robust comparison. We argue that this limitation also precludes a robust assessment of a palaeo-connection between the Yangtze/ Salween/Mekong and the Red River; it is difficult to unequivocally interpret the recorded provenance changes as the result of specific drainage reorganisations. We highlight the palaeo-Red River deposits of the Hanoi Basin as a potential location for future research focus in view of the near-complete Cenozoic record of palaeo-Red River deposits at this location. A majority of previous studies consider that if a major continental-scale drainage ever existed at all, it fragmented early in the Cenozoic. Such a viewpoint would agree with the growing body of evidence from palaeoaltitude studies that large parts of SE Tibet were uplifted by this period. This then leads towards the intriguing question as to the mechanisms which caused the major period of river incision in the Miocene in this region.}, 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{LiShenZhangetal.2022, author = {Li, Jian and Shen, Jinhua and Zhang, Xiaoli and Peng, Yangqin and Zhang, Qin and Hu, Liang and Reichetzeder, Christoph and Zeng, Suimin and Li, Jing and Tian, Mei and Gong, Fei and Lin, Ge and Hocher, Berthold}, title = {Risk factors associated with preterm birth after IVF/ICSI}, series = {Scientific reports}, volume = {12}, journal = {Scientific reports}, number = {1}, publisher = {Nature Research}, address = {Berlin}, issn = {2045-2322}, doi = {10.1038/s41598-022-12149-w}, pages = {9}, year = {2022}, abstract = {In vitro fertilization/intracytoplasmic sperm injection (IVF/ICSI) is associated with an increased risk of preterm (33rd-37th gestational week) and early preterm birth (20th-32nd gestational week). The underlying general and procedure related risk factors are not well understood so far. 4328 infertile women undergoing IVF/ICSI were entered into this study. The study population was divided into three groups: (a) early preterm birth group (n = 66), (b) preterm birth group (n = 675) and (c) full-term birth group (n = 3653). Odds for preterm birth were calculated by stepwise multivariate logistic regression analysis. We identified seven independent risk factors for preterm birth and four independent risk factors for early preterm birth. Older (> 39) or younger (< 25) maternal age (OR: 1.504, 95\% CI 1.108-2.042, P = 0.009; OR: 2.125, 95\% CI 1.049-4.304, P = 0.036, respectively), multiple pregnancy (OR: 9.780, 95\% CI 8.014-11.935, P < 0.001; OR: 8.588, 95\% CI 4.866-15.157, P < 0.001, respectively), placenta previa (OR: 14.954, 95\% CI 8.053-27.767, P < 0.001; OR: 16.479, 95\% CI 4.381-61.976, P < 0.001, respectively), and embryo reduction (OR: 3.547, 95\% CI 1.736-7.249, P = 0.001; OR: 7.145, 95\% CI 1.990-25.663, P = 0.003, respectively) were associated with preterm birth and early preterm birth, whereas gestational hypertension (OR: 2.494, 95\% CI 1.770-3.514, P < 0.001), elevated triglycerides (OR: 1.120, 95\% CI 1.011-1.240, P = 0.030) and shorter activated partial thromboplastin time (OR: 0.967, 95\% CI 0.949-0.985, P < 0.001) were associated only with preterm birth. In conclusion, preterm and early preterm birth risk factors in patients undergoing assisted IVF/ICSI are in general similar to those in natural pregnancy. The lack of some associations in the early preterm group was most likely due to the lower number of early preterm birth cases. Only embryo reduction represents an IVF/ICSI specific risk factor.}, language = {en} }