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Biography
Biography

Editor-in-Chief of OBM Hepatology and Gastroenterology

Osamu Yokosuka is an Emeritus Professor of Chiba University, Japan. He graduated from Chiba University School of Medicine in 1975 then worked as a trainee under Professor K. Okuda in Chiba University Hospital till 1978. Dr. Yokosuka was a research fellow worked under Professor S. Scherlock and Professor B. H. Billing in Royal Free Hospital, London, UK from 1978 to 1980; under Professor M. Omata in Chiba University from 1980 to 1985; and under Dr. J Summers in Fox Chase Cancer Center, PA, USA in 1984. In 1985, he received a Degree of Doctor of Medical Science, and served as an Assistant Professor in Chiba University till 1994, then as Lecturer in Medicine till 2006 when he was appointed as Director and Professor of Medicine. From 2013 to 2015, he served as the Dean of Chiba University School of Medicine.

Dr. Yokosuka was the Secretary General of APASL (2008-2014). In 2016, he was elected as the President of APASL Tokyo, the President of 52nd Annual Meeting of Japan Society of Hepatology, and the President of Funabashi Central Hospital. Dr. Yokosuka’s research mainly focuses on Hepatitis and Hepatocellular Carcinoma. So far, he has published more than 700 original papers.

Biography

The Associate Editor of OBM Hepatology and Gastroenterology

Tatsuo Kanda received a medical degree in 1991 at Niigata University School of Medicine, Japan, and his PhD in 1999 at Chiba University Graduate School of Medicine, Japan. He had post-doctor training for 3 years under Prof. Ratna Ray and Prof. Ranjit Ray at Saint Louis University, St. Louis, MO, USA. In Dec. 2008, Tatsuo Kanda became a Tenure-track Associate Professor at Department of Medicine and Clinical Oncology, Chiba University, Graduate School of Medicine, Japan. In Feb. 2013, Tatsuo Kanda was nominated a permanent Associate Professor at Department of Gastroenterology and Nephrology, Chiba University, Graduate School of Medicine, Japan. In 2017, Tatsuo Kanda became an Associate Professor, Division of Gastroenterology and Hepatology, Department of Internal Medicine, Nihon University School of Medicine. For ~25 years, he has focused his scientific interests on the topics related to liver diseases including acute liver failure, viral hepatitis and autoimmune liver diseases, and worked with Prof. Osamu Yokosuka. Tatsuo Kanda is also an expert for hepatitis A virus (HAV), HBV and HCV, and translation and replication of these viruses, and hepatocarcinogenesis. With his expertise in antiviral therapies and hepatitis virus research, Tatsuo Kanda also sees a lot of patients in clinical daily practice. Tatsuo Kanda has published more than 200 articles in peer-reviewed Journal.

Special Issue

Non-protein-coding RNAs: Novel Mediators in the Pathophysiology of Substance Use Disorders

Submission Deadline: March 10, 2018 (Open)               Submit Now

About This Topic

Background

The societal, economic and human costs due to the use and abuse of psychoactive substances are high. Moreover, despite decades of research, our ability to treat substance use disorders (SUDs) and their consequences is limited. This is partly because the pathophysiology of SUDs is complex. Psychoactive substances like alcohol, nicotine and opiates are often initially used to minimize the aversive effects of mental health states like anxiety and depression. These mental health states themselves persistently if not permanently modify brain circuits. However, excessive substance use and abuse can in turn persistently reprogram core brain circuits, leading to drug tolerance and dependence and the emergence of SUDs. Importantly, many psychoactive drugs have broader adverse effects on other physiological systems, resulting in organ toxicity, cancer and increased susceptibility to metabolic and cardiovascular disease. Finally, several psychoactive substances including alcohol and nicotine are also teratogens. Their presence during critical periods of fetal development can lead to multi-system developmental disabilities. ‘Epigenetics’, the heritable changes in gene expression without changes in DNA, is a core concept that links mental health to SUDs and their pathophysiology. In this issue, we will explore the contribution of non-protein-coding RNAs (ncRNAs) to the epigenetics and pathophysiology of SUDs.

Scope

The human genome is predicted to encode ~19,000 protein coding genes, but nevertheless contains an estimated 1 million transcription start sites, including an estimated 371,849 intergenic transcription start sites. It is become increasingly clear that most of the transcription activity in cells results in the generation of ncRNAs and not protein-coding mRNAs. Over the last 10 years, and increasing number of ncRNAs have been linked to the genesis and outcomes of SUDs. NcRNAs can range in size from large, several kilobases in length (lncRNA), to small (< 200 nucleotides in length). The linkage between some ncRNAs and epigenetics is direct. For instance, the X chromosome inactivating factor, XIST, and PIWI-associated RNAs, piRNAs, both result in chromatin remodeling and inactivation. Other lncRNAs like HOTAIR, H19 and BDNFAS are similarly linked to chromatin remodeling and inactivation. In contrast, other ncRNAs have a more complex role in modifying the transcription output of the genome. Circular RNAs have recently been implicated in the control of splicing machinery, and other lncRNAs in ribosome assembly. Finally, small ncRNAs like microRNAs, miRNAs, play an important role in regulating translation of protein coding mRNAs, but may also engage in RNA-mediated transcriptional silencing.

SUDs and their underlying mental health states have increasingly been shown to recruit a network of ncRNAs within cells and tissues. The epigenetic roles of these ncRNAs are likely to persistently reprogram the transcriptional output of the genome in vulnerable cells and tissues resulting in pathophysiology and treatment resistance. Consequently, while this issue will focus on ncRNAs, its sope will be broad, covering ncRNA contribution to underlying mental health states that facilitate SUDs, the reprogramming of brain networks in SUDs, as well as organ system pathophysiology and teratology associated with SUDs. Primary research reports and review articles are welcome in all areas pertinent to ncRNAs and SUDs. Of particular interest are studies or reviews that focus on manipulating ncRNAs to intervene in the development and pathophysiology of SUDs.