Editors Choice Article | Small Animal Models for Human Immunodeficiency Virus (HIV), Hepatitis B, and Tuberculosis: Proceedings of an NIAID Workshop

Journal Name: Current HIV Research

Author(s): Ramesh Akkina, Daniel L. Barber, Moses T. Bility, Karl-Dimiter Bissig, Benjamin J. Burwitz, Katrin Eichelberg, Janice J. Endsley, J. Victor Garcia, Richard Hafner, Petros C. Karakousis, Brent E. Korba, Rajen Koshy, Chris Lambros, Stephan Menne, Eric L. Nuermberger, Alexander Ploss, Brendan K. Podell, Larisa Y. Poluektova, Brigitte E. Sanders-Beer*, Selvakumar Subbian, Angela Wahl.

 

 

 

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Abstract:

The main advantage of animal models of infectious diseases over in vitro studies is the gain in the understanding of the complex dynamics between the immune system and the pathogen. While small animal models have practical advantages over large animal models, it is crucial to be aware of their limitations. Although the small animal model at least needs to be susceptible to the pathogen under study to obtain meaningful data, key elements of pathogenesis should also be reflected when compared to humans. Welldesigned small animal models for HIV, hepatitis viruses and tuberculosis require, additionally, a thorough understanding of the similarities and differences in the immune responses between humans and small animals and should incorporate that knowledge into the goals of the study. To discuss these considerations, the NIAID hosted a workshop on ‘Small Animal Models for HIV, Hepatitis B, and Tuberculosis’ on May 30, 2019. Highlights of the workshop are outlined below.

 

To read out more, please visit: http://www.eurekaselect.com/177698/article

Become a Reviewer | Current Alzheimer Research (CAR)

 

Current Alzheimer Research publishes peer-reviewed frontier review, research, drug clinical trial studies and letter articles on all areas of Alzheimer’s disease. This multidisciplinary journal will help in understanding the neurobiology, genetics, pathogenesis, and treatment strategies of Alzheimer’s disease. The journal publishes objective reviews written by experts and leaders actively engaged in research using cellular, molecular, and animal models. The journal also covers original articles on recent research in fast emerging areas of molecular diagnostics, brain imaging, drug development and discovery, and clinical aspects of Alzheimer’s disease. Manuscripts are encouraged that relate to the synergistic mechanism of Alzheimer’s disease with other dementia and neurodegenerative disorders. Book reviews, meeting reports and letters-to-the-editor are also published. The journal is essential reading for researchers, educators and physicians with interest in age-related dementia and Alzheimer’s disease. Current Alzheimer Research provides a comprehensive ‘bird’s-eye view’ of the current state of Alzheimer’s research for neuroscientists, clinicians, health science planners, granting, caregivers and families of this devastating disease.

 

Abstracted and Indexed in:

  • Science Citation Index-Expanded
  • Journal Citation Reports/Science Edition
  • InCites
  • Neuroscience Citation Index
  • Current Contents® – Life Sciences
  • Current Contents® – Clinical Medicine
  • BIOSIS
  • BIOSIS Previews
  • BIOSIS Reviews Reports and Meetings
  • MEDLINE/PubMed/Index Medicus
  • Scopus
  • EMBASE
  • Chemical Abstracts Service/SciFinder
  • PsycINFO
  • ProQuest
  • ChemWeb
  • Google Scholar
  • BIOBASE
  • EMNursing
  • EMCare
  • Alzforum
  • MediaFinder®-Standard Periodical Directory
  • Genamics JournalSeek
  • PubsHub
  • Index Copernicus
  • J-Gate
  • CNKI Scholar
  • Suweco CZ
  • TOC Premier
  • EBSCO
  • British Library
  • Ulrich’s Periodicals Directory
  • JournalTOCs

 

The Journal is interested in appointing active Reviewers on the Journal’s Board. If you are working in the mentioned field of the journal and are interested in becoming a Reviewer, send us your CV at the below mentioned email. If, however, the scope of the journal is not directly related to your field of interest then please feel free to recommend suitable colleagues for the Reviewers of the journal and, if possible, send us their CV mentioning the field of interest.

 

Please submit the CV at your earliest convenience at hermain@benthamscience.netand CC faizan@benthamscience.net, mentioning in the subject line your field of interest. The responsibilities of Reviewers will be discussed in detail further once the CV is received.

 

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Become an Editorial Board Member (EBM) | Current Alzheimer Research (CAR)

 

Current Alzheimer Research publishes peer-reviewed frontier review, research, drug clinical trial studies and letter articles on all areas of Alzheimer’s disease. This multidisciplinary journal will help in understanding the neurobiology, genetics, pathogenesis, and treatment strategies of Alzheimer’s disease. The journal publishes objective reviews written by experts and leaders actively engaged in research using cellular, molecular, and animal models. The journal also covers original articles on recent research in fast emerging areas of molecular diagnostics, brain imaging, drug development and discovery, and clinical aspects of Alzheimer’s disease. Manuscripts are encouraged that relate to the synergistic mechanism of Alzheimer’s disease with other dementia and neurodegenerative disorders. Book reviews, meeting reports and letters-to-the-editor are also published. The journal is essential reading for researchers, educators and physicians with interest in age-related dementia and Alzheimer’s disease. Current Alzheimer Research provides a comprehensive ‘bird’s-eye view’ of the current state of Alzheimer’s research for neuroscientists, clinicians, health science planners, granting, caregivers and families of this devastating disease.

 

Abstracted and Indexed in:

  • Science Citation Index-Expanded
  • Journal Citation Reports/Science Edition
  • InCites
  • Neuroscience Citation Index
  • Current Contents® – Life Sciences
  • Current Contents® – Clinical Medicine
  • BIOSIS
  • BIOSIS Previews
  • BIOSIS Reviews Reports and Meetings
  • MEDLINE/PubMed/Index Medicus
  • Scopus
  • EMBASE
  • Chemical Abstracts Service/SciFinder
  • PsycINFO
  • ProQuest
  • ChemWeb
  • Google Scholar
  • BIOBASE
  • EMNursing
  • EMCare
  • Alzforum
  • MediaFinder®-Standard Periodical Directory
  • Genamics JournalSeek
  • PubsHub
  • Index Copernicus
  • J-Gate
  • CNKI Scholar
  • Suweco CZ
  • TOC Premier
  • EBSCO
  • British Library
  • Ulrich’s Periodicals Directory
  • JournalTOCs

 

The Journal is interested in appointing active Editorial Board Members on the Journal’s Board. If you are working in the mentioned field of the journal and are interested in becoming an Editorial Board Member, please send us your CV and a list of publications to the email mentioned below. If, however, the scope of the journal is not directly related to your field of interest then please feel free to recommend suitable colleagues for the Editorial Board membership of the journal and, if possible, send us their CV along with their list of publications.

 

Please submit the CV at your earliest convenience at hermain@benthamscience.netand CC faizan@benthamscience.net, mentioning in the subject line your field of interest. The responsibilities of Editorial Board Members will be discussed in detail further once the CV is received.

 

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Aims & Scope – Current Gene Therapy

Aims & Scope

 

Current Gene Therapy is a bi-monthly peer-reviewed journal aimed at academic and industrial scientists with an interest in major topics concerning basic research and clinical applications of gene and cell therapy of diseases. Cell therapy manuscripts can also include application in diseases when cells have been genetically modified. Current Gene Therapy publishes reviews and original research on the latest developments in gene transfer and gene expression analysis, vector development, cellular genetic engineering, animal models and human clinical applications of gene and cell therapy for the treatment of diseases.

Current Gene Therapy publishes reviews and original research containing experimental data on gene and cell therapy. The journal also includes manuscripts on technological advances, ethical and regulatory considerations of gene and cell therapy. Reviews should provide the reader with a comprehensive assessment of any area of experimental biology applied to molecular medicine that is not only of significance within a particular field of gene therapy and cell therapy but also of interest to investigators in other fields. Authors are encouraged to provide their own assessment and vision for future advances. Reviews are also welcome on late breaking discoveries on which substantial literature has not yet been amassed. Such reviews provide a forum for sharply focused topics of recent experimental investigations in gene therapy primarily to make these results accessible to both clinical and basic researchers. Manuscripts containing experimental data should be original data, not previously published.

 

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For more details, please visit: https://benthamscience.com/journals/current-gene-therapy/aims-scope/#top

PRESS RELEASE – Study reveals potential biomarkers of cerebral aneurysm risk

“The article by Dr. Todd A. Abruzzo et al. is published in Current Neurovascular Research, 2018″

 

Expansive arterial remodeling (EAR) comprises a genetically programmed biological response designed to restore homeostatic levels of arterial wall stress after an increase in vessel flow load occurs. The magnitude and rate of EAR reactions relative to local hemodynamic stress fields and the tensile strength of vascular tissue determines whether the process will result in a stable mural structure (adaptive remodeling) or an unstable mural structure that progresses to form an aneurysm (maladaptive remodeling). A recent study published in Current Neurovascular Research reveals the molecular mechanisms underlying adaptive and maladaptive remodeling of cerebral arteries for the first time.

In this study, investigators flow loaded the basilar artery in rats by performing bilateral carotid artery ligation. Flow induced changes in basilar artery morphometry and histology were correlated with changes in mRNA expression and protein expression. Flow induced alterations in mural structure and biology were revealed by comparison of flow loaded basilar arteries with basilar arteries from rats that underwent sham surgery. The adaptive and maladaptive remodeling responses were differentiated by comparing the results from an aneurysm prone inbred strain of rats to an aneurysm resistant inbred strain of rats. The study revealed 24 genes that were differentially expressed between strains in the absence of flow loading (resting state). More than half of these genes have previously been associated with pathological vascular phenotypes, and more than a third have specifically been associated with aneurysmal pathology.

Numerous flow-induced genes were revealed by this study, including a group of 8 genes that showed very strong flow induced expression conserved in both inbred strains. A group of 9 genes showed very strong flow induced expression with major differences between aneurysm prone inbred rats and the aneurysm resistant inbred rats. These genes are considered to play major roles in maladaptive cerebrovascular remodeling responses that lead to mural destabilization and cerebral aneurysm formation. Three of these genes including the Tgfb3, Ldha and Rgs16 genes have specifically been associated with aneurysmal pathology in prior studies.

The newly discovered maladaptive cerebrovascular remodeling genes revealed by this research may enable the development of new diagnostic biomarker tests for patients at increased risk of cerebral aneurysm formation. Such tests may be used to identify patients at risk for cerebral aneurysm formation at a very early stage. In such cases, it may be possible to stabilize or reverse the aneurysm forming process with targeted therapies before clinical complications occur. The products of maladaptive cerebrovascular remodeling genes may eventually prove to be high yield drug targets for targeted arterial wall stabilizing therapies. Such therapies may be particularly beneficial for individuals at high risk of aneurysm formation, including patients with severe hypertension, unilateral carotid artery occlusions, cerebral arteriovenous malformations and aneurysmal cerebral arteriopathies such as Tuberous Sclerosis, Alagille syndrome and Sickle cell disease.

 

For more information, please visit: http://www.eurekaselect.com/163726/article 

Scholarly Publications by Japanese Authors in BSP Journal: CNS & Neurological Disorders – Drug Targets

CNS & Neurological Disorders – Drug TargetsImage

Biosynthetic Pathways of Bioactive N-Acylethanolamines in Brain

Author(s): Kazuhito Tsuboi, Natsuki Ikematsu, Toru Uyama, Dale G. Deutsch, Akira Tokumura and Natsuo Ueda

Affiliation: Department of Biochemistry, Kagawa University School of Medicine, 1750-1 Ikenobe, Miki, Kagawa 761-0793, Japan.

Abstract

Ethanolamides of long-chain fatty acids are a class of endogenous lipid mediators generally referred to as Nacylethanolamines (NAEs). NAEs include anti-inflammatory and analgesic palmitoylethanolamide, anorexic oleoylethanolamide, and the endocannabinoid anandamide. Since the endogenous levels of NAEs are principally regulated by enzymes responsible for their biosynthesis and degradation, these enzymes are expected as targets for the development of therapeutic agents. Thus, a better understanding of these enzymes is indispensable. The classic “N-acylationphosphodiesterase pathway” for NAE biosynthesis is composed of two steps; the formation of Nacylphosphatidylethanolamine (NAPE) by N-acyltransferase and the release of NAE from NAPE by NAPE-hydrolyzing phospholipase D (NAPE-PLD). However, recent studies, including the analysis of NAPE-PLD-deficient (NAPE-PLD-/-) mice, revealed the presence of NAPE-PLD-independent multi-step pathways to form NAEs from NAPE in animal tissues. Our recent studies using NAPE-PLD-/- mice also suggest that NAE is formed not only from NAPE, but also from Nacylated plasmalogen-type ethanolamine phospholipid (N-acyl-plasmenylethanolamine) through both NAPE-PLDdependent and -independent pathways. Here, we present recent findings on NAE biosynthetic pathways mainly occurring in the brain.

 
 
Author(s): Saki Shimizu, Yuto Mizuguchi and Yukihiro Ohno

Affiliation: Laboratory of Pharmacology, OsakaUniversity of Pharmaceutical Sciences, 4-20-1 Nasahara, Takatsuki, Osaka 569-1094, Japan.

Abstract

Patients with schizophrenia exhibit various clinical symptoms including positive and negative symptoms, neurocognitive impairments and mood disturbances. Although a series of second generation antipsychotics (SGAs) (e.g., risperidone, olanzapine and quetiapine) have been developed in the past two decades, clinical reports do not necessarily show advantages over first generation antipsychotics (FGAs) in the treatment of schizophrenia, especially in their efficacy against cognitive impairment and ability to cause extrapyramidal side effects (EPS). Recently, several lines of studies have revealed therapeutic roles of 5-HT receptors in modulating cognitive impairments and extrapyramidal motor disorders. Specifically, inhibition of 5-HT1A, 5-HT3 and 5-HT6 receptors or activation of 5-HT4 receptors alleviates cognitive impairments (e.g., deficits in learning and memory). In addition, stimulation of 5-HT1A receptors or inhibition of 5-HT3and 5-HT6 receptors as well as 5-HT2A/2C receptors can ameliorate extrapyramidal motor disorders. Thus, controlling the activity of 5-HT1A, 5-HT3 or 5-HT6receptors seems to provide benefits by both alleviating cognitive impairments and reducing antipsychotic-induced EPS. This article reviews the functional roles and mechanisms of 5-HT receptors in the treatment of schizophrenia, focusing on the serotonergic modulation of cognitive and extrapyramidal motor functions, and illustrates future therapeutic strategies.

 

Beyond Rodent Models of Pain: Non-Human Primate Models for Evaluating Novel Analgesic Therapeutics and Elaborating Pain Mechanisms

Author(s): Aldric T. Hama, Katsuo Toide and Hiroyuki Takamatsu

Affiliation: Hamamatsu Pharma Research, Kita-ku, 1-3-7 Shinmiyakoda, Hamamatsu 431-2103, Japan.

Abstract

Evaluation of potential analgesic therapeutics and the elaboration of the neurobiology of pain have heavily relied on pain models developed in rodents. However, a limitation of rodents is their phylogenetic distance from humans, which could in part account for the failure of some preclinical findings to translate to clinical utility. By contrast, given their genetic closeness and phenotypic similarities to humans, it is suggested that there be greater utilization of non-human primates (NHP) in preclinical pain studies. Methods to induce chronic pain-like states and quantify changes in nociception that have been developed in rodents could be adapted to the NHP. Similarly, human experimental injury-induced sensitization, which attempts to temporarily mimic the neuropathology and symptoms observed in the chronic pain state, could be adapted to the NHP. The NHP could then serve as a platform to validate human experimental models as well as proof-of-concept studies. Beyond experimentally modeled pain states, a number of naturally occurring disease states, such as osteoarthritis, are expressed by NHP, which could be utilized for both hypothesis testing and proof-of-concept studies. While NHP studies are logistically cumbersome, it is envisioned that NHP pain models will add value to current preclinical data and greatly facilitate the discovery of novel analgesic treatments.

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