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Institution

University of Tokushima

EducationTokushima, Japan
About: University of Tokushima is a education organization based out in Tokushima, Japan. It is known for research contribution in the topics: Population & Cell culture. The organization has 17219 authors who have published 30742 publications receiving 638753 citations. The organization is also known as: Tokushima Daigaku.


Papers
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Journal ArticleDOI
Daniel J. Klionsky1, Kotb Abdelmohsen2, Akihisa Abe3, Joynal Abedin4  +2519 moreInstitutions (695)
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Abstract: In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure flux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation, it is imperative to target by gene knockout or RNA interference more than one autophagy-related protein. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways implying that not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular assays, we hope to encourage technical innovation in the field.

5,187 citations

Journal ArticleDOI
21 Jan 2011-Science
TL;DR: Oral inoculation of Clostridium during the early life of conventionally reared mice resulted in resistance to colitis and systemic immunoglobulin E responses in adult mice, suggesting a new therapeutic approach to autoimmunity and allergy.
Abstract: CD4+ T regulatory cells (Tregs), which express the Foxp3 transcription factor, play a critical role in the maintenance of immune homeostasis. Here, we show that in mice, Tregs were most abundant in the colonic mucosa. The spore-forming component of indigenous intestinal microbiota, particularly clusters IV and XIVa of the genus Clostridium, promoted Treg cell accumulation. Colonization of mice by a defined mix of Clostridium strains provided an environment rich in transforming growth factor–β and affected Foxp3+ Treg number and function in the colon. Oral inoculation of Clostridium during the early life of conventionally reared mice resulted in resistance to colitis and systemic immunoglobulin E responses in adult mice, suggesting a new therapeutic approach to autoimmunity and allergy.

3,096 citations

Journal ArticleDOI
Peter Goldstraw1, Kari Chansky, John Crowley, Ramón Rami-Porta2, Hisao Asamura3, Wilfried Ernst Erich Eberhardt4, Andrew G. Nicholson1, Patti A. Groome5, Alan Mitchell, Vanessa Bolejack, David Ball6, David G. Beer7, Ricardo Beyruti8, Frank C. Detterbeck9, Wilfried Eberhardt4, John G. Edwards10, Françoise Galateau-Salle11, Dorothy Giroux12, Fergus V. Gleeson13, James Huang14, Catherine Kennedy15, Jhingook Kim16, Young Tae Kim17, Laura Kingsbury12, Haruhiko Kondo18, Mark Krasnik19, Kaoru Kubota20, Antoon Lerut21, Gustavo Lyons, Mirella Marino, Edith M. Marom22, Jan P. van Meerbeeck23, Takashi Nakano24, Anna K. Nowak25, Michael D Peake26, Thomas W. Rice27, Kenneth E. Rosenzweig28, Enrico Ruffini29, Valerie W. Rusch14, Nagahiro Saijo, Paul Van Schil23, Jean-Paul Sculier30, Lynn Shemanski12, Kelly G. Stratton12, Kenji Suzuki31, Yuji Tachimori32, Charles F. Thomas33, William D. Travis14, Ming-Sound Tsao34, Andrew T. Turrisi35, Johan Vansteenkiste21, Hirokazu Watanabe, Yi-Long Wu, Paul Baas36, Jeremy J. Erasmus22, Seiki Hasegawa24, Kouki Inai37, Kemp H. Kernstine38, Hedy L. Kindler39, Lee M. Krug14, Kristiaan Nackaerts21, Harvey I. Pass40, David C. Rice22, Conrad Falkson5, Pier Luigi Filosso29, Giuseppe Giaccone41, Kazuya Kondo42, Marco Lucchi43, Meinoshin Okumura44, Eugene H. Blackstone27, F. Abad Cavaco, E. Ansótegui Barrera, J. Abal Arca, I. Parente Lamelas, A. Arnau Obrer45, R. Guijarro Jorge45, D. Ball6, G.K. Bascom46, A. I. Blanco Orozco, M. A. González Castro, M.G. Blum, D. Chimondeguy, V. Cvijanovic47, S. Defranchi48, B. de Olaiz Navarro, I. Escobar Campuzano2, I. Macía Vidueira2, E. Fernández Araujo49, F. Andreo García49, Kwun M. Fong, G. Francisco Corral, S. Cerezo González, J. Freixinet Gilart, L. García Arangüena, S. García Barajas50, P. Girard, Tuncay Göksel, M. T. González Budiño51, G. González Casaurrán50, J. A. Gullón Blanco, J. Hernández Hernández, H. Hernández Rodríguez, J. Herrero Collantes, M. Iglesias Heras, J. M. Izquierdo Elena, Erik Jakobsen, S. Kostas52, P. León Atance, A. Núñez Ares, M. Liao, M. Losanovscky, G. Lyons, R. Magaroles53, L. De Esteban Júlvez53, M. Mariñán Gorospe, Brian C. McCaughan15, Catherine J. Kennedy15, R. Melchor Íñiguez54, L. Miravet Sorribes, S. Naranjo Gozalo, C. Álvarez de Arriba, M. Núñez Delgado, J. Padilla Alarcón, J. C. Peñalver Cuesta, Jongsun Park16, H. Pass40, M. J. Pavón Fernández, Mara Rosenberg, Enrico Ruffini29, V. Rusch14, J. Sánchez de Cos Escuín, A. Saura Vinuesa, M. Serra Mitjans, Trond Eirik Strand, Dragan Subotic, S.G. Swisher22, Ricardo Mingarini Terra8, Charles R. Thomas33, Kurt G. Tournoy55, P. Van Schil23, M. Velasquez, Y.L. Wu, K. Yokoi 
Imperial College London1, University of Barcelona2, Keio University3, University of Duisburg-Essen4, Queen's University5, Peter MacCallum Cancer Centre6, University of Michigan7, University of São Paulo8, Yale University9, Northern General Hospital10, University of Caen Lower Normandy11, Fred Hutchinson Cancer Research Center12, University of Oxford13, Memorial Sloan Kettering Cancer Center14, University of Sydney15, Sungkyunkwan University16, Seoul National University17, Kyorin University18, University of Copenhagen19, Nippon Medical School20, Katholieke Universiteit Leuven21, University of Texas MD Anderson Cancer Center22, University of Antwerp23, Hyogo College of Medicine24, University of Western Australia25, Glenfield Hospital26, Cleveland Clinic27, Icahn School of Medicine at Mount Sinai28, University of Turin29, Université libre de Bruxelles30, Juntendo University31, National Cancer Research Institute32, Mayo Clinic33, University of Toronto34, Sinai Grace Hospital35, Netherlands Cancer Institute36, Hiroshima University37, City of Hope National Medical Center38, University of Chicago39, New York University40, Georgetown University41, University of Tokushima42, University of Pisa43, Osaka University44, University of Valencia45, Good Samaritan Hospital46, Military Medical Academy47, Fundación Favaloro48, Autonomous University of Barcelona49, Complutense University of Madrid50, University of Oviedo51, National and Kapodistrian University of Athens52, Rovira i Virgili University53, Autonomous University of Madrid54, Ghent University55
TL;DR: The methods used to evaluate the resultant Stage groupings and the proposals put forward for the 8th edition of the TNM Classification for lung cancer due to be published late 2016 are described.

2,826 citations

Journal ArticleDOI
TL;DR: In this paper, the authors reported the finding of a chaotic at tractor in a simple three-dimensional autonomous system, which resembles some familiar features from both the Lorenz and Rossler at tractors.
Abstract: This Letter reports the finding of a new chaotic at tractor in a simple three-dimensional autonomous system, which resembles some familiar features from both the Lorenz and Rossler at tractors.

2,443 citations

Journal ArticleDOI
04 Jul 2013-Nature
TL;DR: It is shown that senescence-associated secretory phenotype (SASP) has crucial roles in promoting obesity-associated hepatocellular carcinoma (HCC) development in mice, and a similar pathway may contribute to at least certain aspects of obesity- associated HCC development in humans as well.
Abstract: Obesity has become more prevalent in most developed countries over the past few decades, and is increasingly recognized as a major risk factor for several common types of cancer. As the worldwide obesity epidemic has shown no signs of abating, better understanding of the mechanisms underlying obesity-associated cancer is urgently needed. Although several events were proposed to be involved in obesity-associated cancer, the exact molecular mechanisms that integrate these events have remained largely unclear. Here we show that senescence-associated secretory phenotype (SASP) has crucial roles in promoting obesity-associated hepatocellular carcinoma (HCC) development in mice. Dietary or genetic obesity induces alterations of gut microbiota, thereby increasing the levels of deoxycholic acid (DCA), a gut bacterial metabolite known to cause DNA damage. The enterohepatic circulation of DCA provokes SASP phenotype in hepatic stellate cells (HSCs), which in turn secretes various inflammatory and tumour-promoting factors in the liver, thus facilitating HCC development in mice after exposure to chemical carcinogen. Notably, blocking DCA production or reducing gut bacteria efficiently prevents HCC development in obese mice. Similar results were also observed in mice lacking an SASP inducer or depleted of senescent HSCs, indicating that the DCA-SASP axis in HSCs has key roles in obesity-associated HCC development. Moreover, signs of SASP were also observed in the HSCs in the area of HCC arising in patients with non-alcoholic steatohepatitis, indicating that a similar pathway may contribute to at least certain aspects of obesity-associated HCC development in humans as well. These findings provide valuable new insights into the development of obesity-associated cancer and open up new possibilities for its control.

1,593 citations


Authors

Showing all 17255 results

NameH-indexPapersCitations
Michael A. Moskowitz13952071904
David H. Pashley13774063657
Kohei Miyazono13551568706
Keiji Tanaka12959482885
Leon O. Chua12282471612
Toshikazu Nakamura12173251374
Akira Yamamoto117199974961
Paul A. Janmey10947348858
Kazuaki Chayama105151152413
Sylvia L. Asa10161139877
John A. Oates9842545285
Akira Kikuchi9341228893
Koji Uchida9142331663
Toshiharu Ninomiya8544935259
Nobutaka Fujii8369528626
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202312
202273
20211,093
20201,096
20191,097
20181,097