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Current issue: 2018
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

On the Role of Early-life Neuroinflammation in Neuropsychiatric Disorders

Submission Deadline: December 30, 2018 (Open)               Submit Now

Guest Editor

Jenny Berrío, MD, MSc
PPG-Ciências da reabilitação, Universidade Federal de Ciências da Saúde de Porto Alegre, Rua Sarmento Leite, 245, Porto Alegre, Brazil
E-Mail: jpaober89@hotmail.com
Website: https://www.escavador.com/sobre/12246268/jenny-paola-berrio-sanchez
https://www.linkedin.com/in/jennypberrios
Research Interests: Behavior; Cognition: Models, animal, Neurodegenerative diseases; Neuronal plasticity; neuro-immune interactions

Co-Editor

Bart Ellenbroek, PhD
Professor and Deputy Head of School, School of Psychology, Victoria University of Wellington, PO Box 600, Wellington 6140, New Zealand
E-Mail: bart.ellenbroek@vuw.ac.nz
Website: http://www.behaviouralneurogenetics.com
Research Interests: animal models; schizophrenia; gene-environment interactions; drug addiction; autism; dopamine; serotonin; behavior

About This Topic

Immune homeostasis within the brain is of special importance for its adequate functioning, thus not surprisingly, any breach of this balance can lead to impaired brain activity. Recent research has identified dysregulated neuroinflammation as a contributing factor in the vulnerability to and development of several neuropsychiatric disorders. In addition to autism and schizophrenia, anxiety and depression, as well as dementia, have now been linked to excessive inflammation of the brain. Particularly, an inappropriate inflammatory response during early-life has been consistently associated with an elevated susceptibility. It has long been known that early-life experiences have the capacity to alter brain development. By changing the long-term function of the immune system, which in turn influences brain function, early-life events have the potential to modify, in the long-term, how the brain is shaped and how it responds to other environmental challenges. The aim of this special issue is to publish up-to-date scientific literature on the topic, deepening the understanding of the complex mechanisms through which this brain-immune connection stresses out our mental health. Original research reports, review articles, communications, and perspectives are welcome in all areas pertinent to the topic. All accepted papers will be published totally free of charge.

Planned Papers

Title: Temporal Lobe Epilepsy, Stroke, and Traumatic Brain Injury: Mechanisms of Hyperpolarized, Depolarized, and Flow-through Ion Channels Utilized as Tri-Coordinate Biomarkers of Electrophysiologic Dysfunction
Authors: Gina Sizemore1, Brandon Lucke-Wold2, Charles Rosen2, James W. Simpkins3, Sanjay Bhatia2, Dandan Sun4
Affiliation:
1.Department of Clinical and Translational Science, West Virginia School of Medicine, Morgantown, WV
2.Department of Neurosurgery, West Virginia School of Medicine, Morgantown, WV
3.Center for Basic and Translational Stroke Research, West Virginia School of Medicine, Morgantown, WV
4.Department of Neurology, University of Pittsburgh, Pittsburgh, PA

Title: Possible roles of transglutaminase 2 in the molecular mechanisms responsible for human neuropsychiatric disorders.
Authors: Nicola Gaetano Gatta, Elenamaria Fioretti and Vittorio Gentile*
Affiliation: Department of Precision Medicine, University of Campania “Luigi Vanvitelli”, via Costantinopoli 16, 80138 Naples, Italy.
Abstract: Transglutaminases are a family of Ca2+-dependent enzymes which catalyze post-translational modifications of proteins. The main activity of these enzymes is the cross-linking of glutaminyl residues of a protein/peptide substrate to lysyl residues of a protein/peptide co-substrate. In addition to lysyl residues, other second nucleophilic co-substrates may include monoamines or polyamines (to form mono- or bi-substituted/crosslinked adducts) or –OH groups (to form ester linkages). In absence of co-substrates, the nucleophile may be water, resulting in the net deamidation of the glutaminyl residue. Transglutaminase activity has been suggested to be involved in molecular mechanisms responsible for both physiological and pathological processes, including inflammation. In particular, transglutaminase 2, a member of the transglutaminase family, has been shown to be responsible for human autoimmune diseases, and Celiac Disease is just one of them. Interestingly, neurodegenerative diseases, such as Alzheimer’s Diseases, Parkinson’s Diseases, supranuclear palsy, Huntington’s Diseases and other polyglutamine diseases, are characterized in part by aberrant cerebral transglutaminase activity and by increased cross-linked proteins in affected brains. In this review we will focus on the possible molecular mechanisms by which this enzyme could be responsible for such diseases and the possible use of transglutaminase inhibitors for patients with neuropsychiatric diseases characterized by aberrant transglutaminase activity.

Title: Vascular plasticity involving AT1 receptors in the amphetamine-induced inflammatory scenario: relevance to animal models of psychiatric disorders.
Authors: Natalia Andrea Marchese 1, Victoria Belén Occhieppo 1, Osvaldo Martin Basmadjian 1, Ana De Paul 2, Gustavo Baiardi 3 and Claudia Bregonzio 1,*
Affiliation:
1. Instituto de Farmacología Experimental Córdoba (IFEC-CONICET) Departamento de Farmacología. Facultad de Ciencias Químicas Universidad Nacional de Córdoba. Córdoba, Argentina
2. Instituto de Investigaciones en Ciencias de la Salud (INICSA- CONICET). Centro de Microscopía Electrónica, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba. Córdoba, Argentina
3. Laboratorio de Neurofarmacología, (IIBYT-CONICET) Universidad Nacional de Córdoba Facultad de Ciencias Químicas, Universidad Católica de Córdoba, Córdoba, Argentina
Abstract:
Amphetamine exposure is validated as a pharmacological tool to model several psychiatric diseases, such as the dopaminergic/glutamatergic imbalance in schizophrenia and mania. However, its effects extend beyond neurotransmission, as psychostimulant exposure has been associated to brain vascular damage and neuroinflammation. AT1 receptors (AT1-R) are implicated in brain micro-vascular physiological responses; whereas their over-expression is related to inflammatory mediators release, oxidative damage, and endothelial dysfunction in pathological conditions. In the present work, we aimed to evaluate amphetamine effects in main brain arteries, and to elucidate AT1-R role in amphetamine-induce alterations in brain micro-vessels. Male adult Wistar rats received amphetamine (2.5mg/kg-i.p., 5 days) and one week later main brain arteries and cerebral-spinal fluid were sampled to assess inflammatory markers. To evaluate AT1-R involvement in amphetamine-induced alterations in brain micro-vessels, AT1-R antagonist (Candesartan; 3mg/kg-p.o., days 1–5) was administered previous to amphetamine administration (days 6–10). One week later (day 17) AT1-R expression at basal conditions and cellular stress after a challenge (angiotensin-II or cold) were assessed. Two-way-ANOVA and Bonferroni test were used. Amphetamine modified carotid structure and increased AT1-R and intercellular-adhesion-molecule-1 expression in middle cerebral artery. Moreover, in cerebral-spinal fluid TNF-α and IL-6 levels were increased after a challenge. In brain micro-vessels, amphetamine increased AT1-R expression and exacerbated heat-shock-protein-70 levels after a challenge. AT1-R blockade prevented AT1-R up-regulation and the sensitized cellular stress responses. Our results stand out vascular plasticity, involving AT1-R, under amphetamine-induced pro-inflammatory conditions.

Title: Does early compositional changes to microflora promote central neuroinflammation in autism?
Authors: Daniel K Goyal 1, Anton Emmanuel 2
Affiliations:
1. Neurosciences Department, University of Manchester, Manchester, England
2. Neurogastroenterology (TBC), University College London, London, United Kingdom

Title: Inflammation in neuronally derived exosomes on psychological outcomes following traumatic brain injury
Authors: Cassandra L Pattinson 1, André van der Merwe 2, Sara Lippa 2, Leighton Chan 2,3,†, Jessica M Gill 1,3,†
Affiliation:
1. National Institute of Nursing Research, National Institutes of Health, Bethesda, MD
2. National Institutes of Health Clinical Center, National Institutes of Health, Bethesda, MD
3. Center for Neuroscience and Regenerative Medicine (CNRM), Uniformed Services University, Bethesda, MD.
† Co-senior authors

Title: Elevated levels of IL-6 alter the progenitor composition of the brain's germinal zones: implications for neuropsychiatric diseases
Authors: Ekta Kumari and Steven W. Levison
Affiliation: Department of Pharmacology, Physiology and Neuroscience, Rutgers-New Jersey Medical School, Newark, NJ, USA

Title: Autoantibodies against cerebellar neurons and phosphatidylethanolamine binding protein-1 in a paediatric patient with stiff-person syndrome and autoimmune polyendocrinopathy type 1
Authors: Carmen Schröder, Natalie Bachmaier, Timothy Howell, Heinz Lauffer, Roman Legrand, Philippe Chan, David Vaudry, Maria Hamze-Sinno, Marie François, Pierre Déchelotte, Tomas Hökfelt, Sergueï O. Fetissov
Abstract:
Stiff-person-syndrome (SPS) is commonly related to autoantibodies against glutamic acid decarboxylase (GAD). Here, putative brain autoantibody targets were studied in GAD autoantibody negative 11-years-old boy with SPS and autoimmune polyendocrine syndrome type 1. We found that at the peak of SPS symptoms, IgG from both patient’s serum and cerebrospinal fluid immunostained cerebellar Golgi cells and neuronal fibers. Using proteomics, phosphatidylethanolamine-binding protein-1 has been identified as the putative autoantigen in the cerebellum. These results show that an unusual case of SPS can be associated with autoimmunity against phosphatidylethanolamine-binding protein-1 and specific brain targets.