Editorial Board
Guoying Bing
Professor Department of Anatomy and Neurobiology Room HSRB 426, College of Medicine · China
Editorial leadership for International Journal of Human Anatomy ISSN 2577-2279
Research interests
- Neuroinflammation &Nbsp; Mediated &Nbsp; Dopaminergic Cell Death Parkinson&Rsquo;S &Nbsp; Disease (Pd) Is A Neurodegenerative Disease Characterized By Loss Of The Dopamine-Containing &Nbsp; Neurons In The Substantia Nigra Pars Compacta (Snpc). Although The Cause Of &Nbsp; Neuronal Death Remains Unclear
- Increasing Evidence Points To The Role Of Chronic &Nbsp; Inflammatory Processes. In Order To Explore The Possibility That Microglial &Nbsp; Activation Causes Dopaminergic Cell Death In The Snpc
- Lipopolysaccharide (Lps)
- &Nbsp; A Bacterial Endotoxin That Activate Microglia
- Was Into The Substantia Nigra &Nbsp; (Sn). The Lps Injection Not Only Caused The Activation Of Microglia
- But Also &Nbsp; Resulted In A Dose-Dependent
- Selective Loss Of Dopaminergic Neurons By Apoptosis &Nbsp; In The Snpc. We Therefore Hypothesize That Lps Activates Microglia In The Sn &Nbsp; Resulting In The Release Of Cytotoxic Agents. These Agents
- In Turn
- Activate &Nbsp; Signal Transduction Pathways That Cause Neuronal Degeneration Of Dopaminergic &Nbsp; Neurons In The Sn. The Long-Term Goal Of This Study Is To Validate Lps Injection &Nbsp; As A New Animal Model Of Pd That Can Be Used To Elucidate The Etiology
- Molecular &Nbsp; Mechanisms Underlying Pd
- To Develop Novel Therapeutic Treatments For This &Nbsp
- Other Neurodegenerative Diseases. Influence Of Xenobiotic &Nbsp; Metabolites On The Neuronal Cell Death &Nbsp; Dr. Bing&Rsquo;S Laboratory Has Recently Found That A High Level Of Microsomal &Nbsp; Epoxide Hydrolase (Meh) Expression In The Brain Of Patients With Alzheimer&Rsquo;S &Nbsp; Disease As Well As The Rat Brain Following Exposure To Neurodegenerative Agents &Nbsp; Such As Kainic Acid
- Trimethyl-Tin. Relatively Little Is Known About The &Nbsp; Expression
- Function Of Meh In The Cns. However
- The Dual Function Of Meh &Nbsp; In The Activation As Well As The Inactivation Of Various Reactive Compounds &Nbsp; From Xenobiotic Metabolites Has Important Implications Regarding Its Role In &Nbsp; Brain Toxicity. The Hypothesize Is That Meh Plays A Crucial Role In The Biotransformation &Nbsp; Of Endogenous Xenobiotics And/Or Environmental Chemicals Into More Toxic Metabolites &Nbsp; Which May Cause Neuronal Degeneration In Specific Neuronal Populations. The &Nbsp; Identifying The Exact Role Of Meh As Well As The Role Of Xenobiotic Metabolites &Nbsp; In The Brain Will Be Critical In Understanding The Neurodegeneration Induced &Nbsp; By Exposure To Toxic Chemicals
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This journal is guided by Guoying Bing (Professor Department of Anatomy and Neurobiology Room HSRB 426, College of Medicine) and a peer-review board of practising researchers. Open access, author-retained copyright (CC BY), and a clear editorial process.