Institution
Hiroshima University
Education•Hiroshima, Japan•
About: Hiroshima University is a education organization based out in Hiroshima, Japan. It is known for research contribution in the topics: Population & Cancer. The organization has 33602 authors who have published 69290 publications receiving 1495648 citations. The organization is also known as: Hiroshima Daigaku.
Topics: Population, Cancer, Gene, Catalysis, Transplantation
Papers published on a yearly basis
Papers
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TL;DR: A striking increase in the incidence of myocardial infarction appears to have occurred in the Japanese who migrated to the United States; this increase is more pronounced in California than in Hawaii.
Abstract: The incidence of myocardial infarction and death from coronary heart disease was studied in defined samples of 45 to 68 year old Japanese men in Japan, Hawaii and California. The incidence rate was lowest in Japan where it was half that observed in Hawaii (P less than 0.01). The youngest men in the sample in Japan were at particularly low risk. The incidence among Japanese men in California was nearly 50 percent greater than that of Japanese in Hawaii (P less than 0.05). A striking increase in the incidence of myocardial infarction appears to have occurred in the Japanese who migrated to the United States; this increase is more pronounced in California than in Hawaii.
469 citations
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TL;DR: The p16INK4a /Rb-pathway also cooperates with mitogenic signals to induce elevated intracellular levels of reactive oxygen species (ROS), thereby activating protein kinase Cδ (PKCδ) in human senescent cells, uncover an unexpected role for the p16ink4a–Rb pathway and provide a new insight into how senescent cell-cycle arrest is enforced in human cells.
Abstract: The p16(INK4a) cyclin-dependent kinase inhibitor has a key role in establishing stable G1 cell-cycle arrest through activating the retinoblastoma (Rb) tumour suppressor protein pRb in cellular senescence. Here, we show that the p16(INK4a) /Rb-pathway also cooperates with mitogenic signals to induce elevated intracellular levels of reactive oxygen species (ROS), thereby activating protein kinase Cdelta (PKCdelta) in human senescent cells. Importantly, once activated by ROS, PKCdelta promotes further generation of ROS, thus establishing a positive feedback loop to sustain ROS-PKCdelta signalling. Sustained activation of ROS-PKCdelta signalling irreversibly blocks cytokinesis, at least partly through reducing the level of WARTS (also known as LATS1), a mitotic exit network (MEN) kinase required for cytokinesis, in human senescent cells. This irreversible cytokinetic block is likely to act as a second barrier to cellular immortalization ensuring stable cell-cycle arrest in human senescent cells. These results uncover an unexpected role for the p16(INK4a)-Rb pathway and provide a new insight into how senescent cell-cycle arrest is enforced in human cells.
469 citations
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TL;DR: The regulation of telomere length and telomerase activity is a complex and dynamic process that is tightly linked to cell cycle regulation in human stem cells.
Abstract: Telomeres, guanine-rich tandem DNA repeats of the chromosomal end, provide chromosomal stability, and cellular replication causes their loss. In somatic cells, the activity of telomerase, a reverse transcriptase that can elongate telomeric repeats, is usually diminished after birth so that the telomere length is gradually shortened with cell divisions, and triggers cellular senescence. In embryonic stem cells, telomerase is activated and maintains telomere length and cellular immortality; however, the level of telomerase activity is low or absent in the majority of stem cells regardless of their proliferative capacity. Thus, even in stem cells, except for embryonal stem cells and cancer stem cells, telomere shortening occurs during replicative ageing, possibly at a slower rate than that in normal somatic cells. Recently, the importance of telomere maintenance in human stem cells has been highlighted by studies on dyskeratosis congenital, which is a genetic disorder in the human telomerase component. The regulation of telomere length and telomerase activity is a complex and dynamic process that is tightly linked to cell cycle regulation in human stem cells. Here we review the role of telomeres and telomerase in the function and capacity of the human stem cells.
469 citations
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TL;DR: The present results suggest that oocyte methylation can be divided into 2 types: Dnmt3L-dependent methylation, which is required for maternal methylation imprinting, and DnMT3 L-independent methylation , which might be essential for endogenous retroviral DNA silencing.
Abstract: Genome-wide dynamic changes in DNA methylation are indispensable for germline development and genomic imprinting in mammals. Here, we report single-base resolution DNA methylome and transcriptome maps of mouse germ cells, generated using whole-genome shotgun bisulfite sequencing and cDNA sequencing (mRNA-seq). Oocyte genomes showed a significant positive correlation between mRNA transcript levels and methylation of the transcribed region. Sperm genomes had nearly complete coverage of methylation, except in the CpG-rich regions, and showed a significant negative correlation between gene expression and promoter methylation. Thus, these methylome maps revealed that oocytes and sperms are widely different in the extent and distribution of DNA methylation. Furthermore, a comparison of oocyte and sperm methylomes identified more than 1,600 CpG islands differentially methylated in oocytes and sperm (germline differentially methylated regions, gDMRs), in addition to the known imprinting control regions (ICRs). About half of these differentially methylated DNA sequences appear to be at least partially resistant to the global DNA demethylation that occurs during preimplantation development. In the absence of Dnmt3L, neither methylation of most oocyte-methylated gDMRs nor intragenic methylation was observed. There was also genome-wide hypomethylation, and partial methylation at particular retrotransposons, while maintaining global gene expression, in oocytes. Along with the identification of the many Dnmt3L-dependent gDMRs at intragenic regions, the present results suggest that oocyte methylation can be divided into 2 types: Dnmt3L-dependent methylation, which is required for maternal methylation imprinting, and Dnmt3L-independent methylation, which might be essential for endogenous retroviral DNA silencing. The present data provide entirely new perspectives on the evaluation of epigenetic markers in germline cells.
468 citations
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Yonsei University1, University of Indonesia2, Aga Khan University3, University of Tartu4, Alfaisal University5, Ziauddin University6, Dubai Health Authority7, Shaikh Zayed Hospital8, Baqiyatallah University of Medical Sciences9, King Saud University10, King Saud bin Abdulaziz University for Health Sciences11, American University of Beirut12, Sungkyunkwan University13, University of Balamand14, Khyber Medical University15, University of Peshawar16, Reykjavík University17, RMIT University18, University of Ljubljana19, La Trobe University20, University of New South Wales21, University of Pécs22, University Medical Center Rizk Hospital23, University of Iceland24, Soonchunhyang University25, Cleveland Clinic26, Vilnius University27, Vilnius Gediminas Technical University28, University of Ulsan29, Tehran University of Medical Sciences30, Aims Community College31, University of Sydney32, Eijkman Institute for Molecular Biology33, Memorial Hospital of South Bend34, Pakistan Institute of Development Economics35, Military Hospital36, Saint Joseph's University37, Allama Iqbal Medical College38, Hiroshima University39, Lahore General Hospital40, Holy Family Hospital41, Rawalpindi Medical College42, Dow Medical College43
TL;DR: The current treatment rate and efficacy are not sufficient to manage the disease burden of hepatitis C virus and alternative strategies are required to keep the number of HCV individuals with advanced liver disease and liver‐related deaths from increasing.
Abstract: The disease burden of hepatitis C virus (HCV) is expected to increase as the infected population ages. A modelling approach was used to estimate the total number of viremic infections, diagnosed, treated and new infections in 2013. In addition, the model was used to estimate the change in the total number of HCV infections, the disease progression and mortality in 2013-2030. Finally, expert panel consensus was used to capture current treatment practices in each country. Using today's treatment paradigm, the total number of HCV infections is projected to decline or remain flat in all countries studied. However, in the same time period, the number of individuals with late-stage liver disease is projected to increase. This study concluded that the current treatment rate and efficacy are not sufficient to manage the disease burden of HCV. Thus, alternative strategies are required to keep the number of HCV individuals with advanced liver disease and liver-related deaths from increasing.
463 citations
Authors
Showing all 33744 results
Name | H-index | Papers | Citations |
---|---|---|---|
Tadamitsu Kishimoto | 181 | 1067 | 130860 |
Takashi Taniguchi | 152 | 2141 | 110658 |
Yasushi Fukazawa | 135 | 882 | 64424 |
Itsuo Nakano | 135 | 1539 | 97905 |
T. Ohsugi | 133 | 664 | 66010 |
Jerry W. Shay | 133 | 639 | 74774 |
Tsunefumi Mizuno | 130 | 478 | 60014 |
Tohru Takeshita | 128 | 1036 | 78625 |
Alex K.-Y. Jen | 128 | 921 | 61811 |
Andreas Kugel | 128 | 910 | 75529 |
Alain Benoit | 124 | 465 | 86284 |
Hiromitsu Takahashi | 124 | 499 | 55976 |
Yoshimi Takai | 122 | 680 | 61478 |
Toshio Hirano | 120 | 401 | 55721 |
Joakim Nystrand | 117 | 658 | 50146 |