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4 citation(s) found for "Wang, Meng".

Symposia Report of The Annual Biological Sciences Section Meeting of the Gerontological Society of America 2023, Tampa, Florida
Rogina, Blanka , Anderson, Rozalyn M. , Curan, Sean, Yousefzadeh, Matthew J. , Ghosh, Bhaswati, Duque, Gustavo , Howlett, Susan E. , Austad, Steven N. , Korfhage, Justin , Christensen, Kaare , Carey, James R. , Bell, Justice, Gomes, Ana P. , Dixit, Vishwa Deep , Sen, Payel , Imai, Shin‐ichiro , Valdez, Gregorio , Orr, Miranda E. , Jones, Leanne , Castillo-Azofeida, David, Bonaguidi, Michael A. , Suh, Yousin , Duncan, Francesca E. , C, Weigler G Perry, Burkewitz, Kristopher , Zhou, Kai , Bouhrara, Mustapha , Kolind, Shannon , Dean, Doug, Pálovics, Róbert , Niedernhofer, Laura J. , Fan, Rong , Bueckle, Andreas , Kapahi, Pankaj , Jiang, Nisi , Diaz, Jose , Mishra, Sidharth P. , Ralmundo, Nuno, Banarjee, Reema , Allsopp, Richard , Curran, Sean P. , Anderson, Rozalyn M , Curran, Sean P , Yousefzadeh, Matthew J , Duque, Gustavo , Howlett, Susan , Austad, Steven , Demuth, Ilja , Gerstorf, Denis , Abadir, Peter , Christensen, Kaare , Palmer, Allyson, Basisty, Nathan , de Cabo, Rafael , Sen, Payel , Baur, Joseph A , Duncan, Francesca E , Benjamini, Dan , Walker, Keenan A , Dean, Douglas C , Gladyshev, Vadim N , Fan, Rong , Sato, Shogo , Jiang, Nisi , Ashiqueali, Sarah A., Allsopp, Richard , Niedernhofer, Laura J , Kollind, Shannon H , LeBrasseur, Nathan K. , Lombard, David B. , Alberts, Susan C. , Campos, Fernando A. , Palavicini, Juan Pablo , Palmer, Allyson K. , Basisty, Nathan , Cabo, Rafael de , Baur, Joseph A. , Li, Xiaoling , Pletcher, Scott D. , Andersen, Julie Kay , Jones, Leanne, Suh, Yousin , Murray, Anna , Wang, Meng C., Henne, W. Mike , Walker, Keenan A. , Reiter, David A. , Gorbunova, Vera , Gladyshev, Vadim N. , Hurley, Jennifer , Esser, Karyn A. , Ashiqueali, Sarah , Reynolds, Lindsay M. , Zhang, Bohan , Sebastiani, Paola , Monti, Stefano , Schork, Nicholas J. , Rappaport, Noa

Mayo Clinic

The Journals of Gerontology, Series A: Biological Sciences and Medical Sciences | February 11, 2025 | Volume: 80 | Issue: 5 | Pages: No page available

10.1093/gerona/glaf026 | PMID 39932386 Get It

Abstract The aging process is universal, and it is characterized by a progressive deterioration and decrease in physiological function leading to decline on the organismal level. Nevertheless, a number of genetic and nongenetic interventions have been described, which successfully extend healthspan and lifespan in different species. Furthermore, a number of clinical trials have been evaluating the feasibility of different interventions to promote human health. The goal of the annual Biological Sciences Section of the Gerontological Society of America meeting was to share current knowledge of different topics in aging research and provide a vision of the future of aging research. The meeting gathered international experts in diverse areas of aging research including basic biology, demography, and clinical and translational studies. Specific topics included metabolism, inflammaging, epigenetic clocks, frailty, senescence, neuroscience, stem cells, reproductive aging, inter-organelle crosstalk, comparative transcriptomics of longevity, circadian clock, metabolomics, and biodemography.
Predictive modeling of spread in adult‐onset isolated dystonia: Key properties and effect of tremor inclusion
Wang, Meng , Morgante, Francesca , Adler, Charles H. , Bäumer, Tobias , Berardelli, Alfredo , Blumin, Joel H. , Borsche, Max , Brashear, Allison , Deik, Andres , Duque, Kevin R. , Feuerstein, Jeanne , Fox, Susan H. , LeDoux, Mark S. , Leegwater‐Kim, Julie, Mahajan, Abhimanyu , Ondo, William G. , Pantelyat, Alexander , Pirio‐Richardson, Sarah, Roze, Emmanuel , Saunders‐Pullman, Rachel , Suchowersky, Oksana , Truong, Daniel , Morgante, Francesca , Adler, C H , Berardelli, Alfredo , Borsche, Max , Mahajan, Abhimanyu , Martino, Davide , Pantelyat, Alex , Sajobi, Tolulope T. , Berman, Brian D. , Espay, Alberto J. , Ferrazzano, Gina , Frank, Samuel , Hallett, Mark , Jankovic, Joseph J. , Malaty, Irene A. , Vidailhet, Marie , Shukla, Aparna Wagle , Perlmutter, Joel S. , Jinnah, H. A.

Mayo Clinic

European Journal of Neurology | July 22, 2021 | Volume: 28 | Issue: 12 | Pages: 3999-4009

10.1111/ene.15031 | PMID 34296504 Get It

AbstractBackground and purposeSeveral clinical and demographic factors relate to anatomic spread of adult‐onset isolated dystonia, but a predictive model is still lacking. The aims of this study were: (i) to develop and validate a predictive model of anatomic spread of adult‐onset isolated dystonia; and (ii) to evaluate whether presence of tremor associated with dystonia influences model predictions of spread.MethodsAdult‐onset isolated dystonia participants with focal onset from the Dystonia Coalition Natural History Project database were included. We developed two prediction models, one with dystonia as sole disease manifestation (“dystonia‐only”) and one accepting dystonia OR tremor in any body part as disease manifestations (“dystonia OR tremor”). Demographic and clinical predictors were selected based on previous evidence, clinical plausibility of association with spread, or both. We used logistic regressions and evaluated model discrimination and calibration. Internal validation was carried out based on bootstrapping.ResultsBoth predictive models showed an area under the curve of 0.65 (95% confidence intervals 0.62–0.70 and 0.62–0.69, respectively) and good calibration after internal validation. In both models, onset of dystonia in body regions other than the neck, older age, depression and history of neck trauma were predictors of spread.ConclusionsThis predictive modeling of spread in adult‐onset isolated dystonia based on accessible predictors (demographic and clinical) can be easily implemented to inform individuals’ risk of spread. Because tremor did not influence prediction of spread, our results support the argument that tremor is a part of the dystonia syndrome, and not an independent or coincidental disorder.
Heterogeneity of meningeal B cells reveals a lymphopoietic niche at the CNS borders
Brioschi, Simone , Wang, Wei-Le , Peng, Vincent , Wang, Meng , Shchukina, Irina, Greenberg, Zev J. , Bando, Jennifer K. , Jaeger, Natália , Czepielewski, Rafael S. , Swain, Amanda , Mogilenko, Denis A. , Beatty, Wandy L. , Fitzpatrick, James A. J. , Schuettpelz, Laura G. , Fronick, Catrina C. , Smirnov, Igor , Kipnis, Jonathan , Wu, Gregory F. , Gilfillan, Susan , Artyomov, Maxim N. , Fitzpatrick, James A J , Fronick, Catrina C , Kipnis, Jonathan , Shapiro, Virginia S , Wu, Gregory F , Gilfillan, Susan , Cella, Marina , Artyomov, Maxim N , Kleinstein, Steven H , Colonna, Marco , Bando, Jennifer K , Brioschi, Simone , Bayguinov, Peter O. , Shapiro, Virginia Smith , Colonna, Marco

Mayo Clinic

Science | June 3, 2021 | Volume: 373 | Issue: 6553 | Pages: No page available

10.1126/science.abf9277 | PMID 34083450 Get It

Getting around the blood–brain barrier The meninges comprise three membranes that surround and protect the central nervous system (CNS). Recent studies have noted the existence of myeloid cells resident there, but little is known about their ontogeny and function, and whether other meningeal immune cell populations have important roles remains unclear (see the Perspective by Nguyen and Kubes). Cugurra et al. found in mice that a large proportion of continuously replenished myeloid cells in the dura mater are not blood derived, but rather transit from cranial bone marrow through specialized channels. In models of CNS injury and neuroinflammation, the authors demonstrated that these myeloid cells have an immunoregulatory phenotype compared with their more inflammatory blood-derived counterparts. Similarly, Brioschi et al. show that the meninges host B cells that are also derived from skull bone marrow, mature locally, and likely acquire a tolerogenic phenotype. They further found that the brains of aging mice are infiltrated by a second population of age-associated B cells, which come from the periphery and may differentiate into autoantibody-secreting plasma cells after encountering CNS antigens. Together, these two studies may inform future treatment of neurological diseases. Science , abf7844, abf9277, this issue p. eabf7844 , p. eabf9277 ; see also abj8183, p. 396
Eosinophils attenuate hepatic ischemia-reperfusion injury in mice through ST2-dependent IL-13 production
Wang, Yaochun , Yang, Yang , Wang, Meng , Wang, Shuhong , Jeong, Jong‐Min , Xu, Long , Wen, Yankai , Emontzpohl, Christoph , Atkins, Constance L. , Duong, Kevin , Moreno, Nicolas F. , Yuan, Xiaoyi , Hall, David R. , Dar, Wasim , Feng, Dechun , Bynon, John S. , Akira, Shizuo , Brown, Jared M. , Jacobsen, Elizabeth A. , Ju, Cynthia, Atkins, Constance Lynn , Xu, Yong , Czigany, Zoltan , Colgan, Sean P , Bynon, J Steve , Jacobsen, Elizabeth A , Ju, Cynthia , Wen, Yankai , Moreno, Nicolas F , Yang, Yang , Gao, Bin , Eltzschig, Holger K.

Mayo Clinic

Science Translational Medicine | February 3, 2021 | Volume: 13 | Issue: 579 | Pages: No page available

10.1126/scitranslmed.abb6576 | PMID 33536281 Get It

Eosinophils protect against liver injury during orthotopic liver transplantation and other conditions of hepatic ischemia-reperfusion injury in mice.