Institution
Fukushima Medical University
Education•Fukushima, Japan•
About: Fukushima Medical University is a education organization based out in Fukushima, Japan. It is known for research contribution in the topics: Population & Cancer. The organization has 3940 authors who have published 8865 publications receiving 171633 citations. The organization is also known as: Fukushima kenritsu ika Daigaku.
Topics: Population, Cancer, Medicine, Heart failure, Fukushima Nuclear Accident
Papers published on a yearly basis
Papers
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University College London1, Children's Hospital of Philadelphia2, VU University Medical Center3, Sir Charles Gairdner Hospital4, National Multiple Sclerosis Society5, Vita-Salute San Raffaele University6, Medical University of Graz7, Ottawa Hospital Research Institute8, Fukushima Medical University9, New York University10, University of Düsseldorf11, University of Basel12, Corinne Goldsmith Dickinson Center for Multiple Sclerosis13, University of Manitoba14, St. Michael's Hospital15, Hebron University16, Johns Hopkins University17, University of Copenhagen18, University of British Columbia19, University of Bari20, Claude Bernard University Lyon 121, French Institute of Health and Medical Research22, University of California, San Francisco23, Mayo Clinic24, Salisbury University25, Cleveland Clinic26
TL;DR: The 2017 McDonald criteria continue to apply primarily to patients experiencing a typical clinically isolated syndrome, define what is needed to fulfil dissemination in time and space of lesions in the CNS, and stress the need for no better explanation for the presentation.
Abstract: The 2010 McDonald criteria for the diagnosis of multiple sclerosis are widely used in research and clinical practice. Scientific advances in the past 7 years suggest that they might no longer provide the most up-to-date guidance for clinicians and researchers. The International Panel on Diagnosis of Multiple Sclerosis reviewed the 2010 McDonald criteria and recommended revisions. The 2017 McDonald criteria continue to apply primarily to patients experiencing a typical clinically isolated syndrome, define what is needed to fulfil dissemination in time and space of lesions in the CNS, and stress the need for no better explanation for the presentation. The following changes were made: in patients with a typical clinically isolated syndrome and clinical or MRI demonstration of dissemination in space, the presence of CSF-specific oligoclonal bands allows a diagnosis of multiple sclerosis; symptomatic lesions can be used to demonstrate dissemination in space or time in patients with supratentorial, infratentorial, or spinal cord syndrome; and cortical lesions can be used to demonstrate dissemination in space. Research to further refine the criteria should focus on optic nerve involvement, validation in diverse populations, and incorporation of advanced imaging, neurophysiological, and body fluid markers.
3,945 citations
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TL;DR: It is found that mice lacking Atg7 specifically in the central nervous system showed behavioural defects, including abnormal limb-clasping reflexes and a reduction in coordinated movement, and died within 28 weeks of birth, and that impairment of autophagy is implicated in the pathogenesis of neurodegenerative disorders involving ubiquitin-containing inclusion bodies.
Abstract: Protein quality-control, especially the removal of proteins with aberrant structures, has an important role in maintaining the homeostasis of non-dividing neural cells. In addition to the ubiquitin-proteasome system, emerging evidence points to the importance of autophagy--the bulk protein degradation pathway involved in starvation-induced and constitutive protein turnover--in the protein quality-control process. However, little is known about the precise roles of autophagy in neurons. Here we report that loss of Atg7 (autophagy-related 7), a gene essential for autophagy, leads to neurodegeneration. We found that mice lacking Atg7 specifically in the central nervous system showed behavioural defects, including abnormal limb-clasping reflexes and a reduction in coordinated movement, and died within 28 weeks of birth. Atg7 deficiency caused massive neuronal loss in the cerebral and cerebellar cortices. Notably, polyubiquitinated proteins accumulated in autophagy-deficient neurons as inclusion bodies, which increased in size and number with ageing. There was, however, no obvious alteration in proteasome function. Our results indicate that autophagy is essential for the survival of neural cells, and that impairment of autophagy is implicated in the pathogenesis of neurodegenerative disorders involving ubiquitin-containing inclusion bodies.
3,349 citations
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TL;DR: The findings highlight the unexpected role of homeostatic level of p62, which is regulated by autophagy, in controlling intracellular inclusion body formation, and indicate that the pathologic process associated with autophagic deficiency is cell-type specific.
2,018 citations
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TL;DR: The findings indicate that the pathological process associated with p62 accumulation results in hyperactivation of Nrf2 and delineates unexpected roles of selective autophagy in controlling the transcription of cellular defence enzyme genes.
Abstract: Impaired selective turnover of p62 by autophagy causes severe liver injury accompanied by the formation of p62-positive inclusions and upregulation of detoxifying enzymes. These phenotypes correspond closely to the pathological conditions seen in human liver diseases, including alcoholic hepatitis and hepatocellular carcinoma. However, the molecular mechanisms and pathophysiological processes in these events are still unknown. Here we report the identification of a novel regulatory mechanism by p62 of the transcription factor Nrf2, whose target genes include antioxidant proteins and detoxification enzymes. p62 interacts with the Nrf2-binding site on Keap1, a component of Cullin-3-type ubiquitin ligase for Nrf2. Thus, an overproduction of p62 or a deficiency in autophagy competes with the interaction between Nrf2 and Keap1, resulting in stabilization of Nrf2 and transcriptional activation of Nrf2 target genes. Our findings indicate that the pathological process associated with p62 accumulation results in hyperactivation of Nrf2 and delineates unexpected roles of selective autophagy in controlling the transcription of cellular defence enzyme genes.
1,918 citations
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The Catholic University of America1, Royal Prince Alfred Hospital2, University of Toronto3, Centre for Addiction and Mental Health4, Università Campus Bio-Medico5, University of Eastern Finland6, Monash University7, Medical University of South Carolina8, Paris 12 Val de Marne University9, University of Regensburg10, University of Brescia11, University of Göttingen12, Beth Israel Deaconess Medical Center13, University of Siena14, University College London15, Copenhagen University Hospital16, Fukushima Medical University17, University of Tübingen18
TL;DR: These guidelines provide an up-date of previous IFCN report on “Non-invasive electrical and magnetic stimulation of the brain, spinal cord and roots: basic principles and procedures for routine clinical application” and include some recent extensions and developments.
1,850 citations
Authors
Showing all 3995 results
Name | H-index | Papers | Citations |
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Hiroaki Shimokawa | 111 | 949 | 48822 |
Jadwiga A. Wedzicha | 104 | 505 | 49160 |
Toshio Miyata | 85 | 374 | 21640 |
George R. Saade | 82 | 872 | 30325 |
Hirotsugu Ueshima | 78 | 597 | 26571 |
Jeffrey Bennett | 76 | 544 | 21098 |
Teizo Fujita | 72 | 229 | 16680 |
Ryuta Kawashima | 71 | 502 | 17005 |
Kunihiko Tamaki | 68 | 519 | 18020 |
Masaharu Nishimura | 67 | 541 | 36086 |
Shunichi Yamashita | 67 | 594 | 18079 |
Ken Okumura | 65 | 561 | 18237 |
Kazuo Fujihara | 65 | 342 | 30314 |
Kenji Kadomatsu | 65 | 347 | 14199 |
Shunichi Fukuhara | 64 | 478 | 18652 |