Animal Models for Computing and Communications: Past Approaches and Future Challenges

2016 ◽  
pp. 21-36
Keyword(s):  
Animal Models ◽  
Future Challenges

scholarly journals The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill

2015 ◽  
Vol 95 (3) ◽  
pp. 1025-1109 ◽  
Author(s):  
O. Friedrich ◽  
M. B. Reid ◽  
G. Van den Berghe ◽  
I. Vanhorebeek ◽  
G. Hermans ◽  
...  
Keyword(s):  
Critical Illness ◽  
Animal Models ◽  
Time Course ◽  
Protein Quality ◽  
Early Mobilization ◽  
Tight Glycemic Control ◽  
Membrane Excitability ◽  
Diagnostic Features ◽  
Future Challenges ◽  
Ubiquitin Proteasome

Critical illness polyneuropathies (CIP) and myopathies (CIM) are common complications of critical illness. Several weakness syndromes are summarized under the term intensive care unit-acquired weakness (ICUAW). We propose a classification of different ICUAW forms (CIM, CIP, sepsis-induced, steroid-denervation myopathy) and pathophysiological mechanisms from clinical and animal model data. Triggers include sepsis, mechanical ventilation, muscle unloading, steroid treatment, or denervation. Some ICUAW forms require stringent diagnostic features; CIM is marked by membrane hypoexcitability, severe atrophy, preferential myosin loss, ultrastructural alterations, and inadequate autophagy activation while myopathies in pure sepsis do not reproduce marked myosin loss. Reduced membrane excitability results from depolarization and ion channel dysfunction. Mitochondrial dysfunction contributes to energy-dependent processes. Ubiquitin proteasome and calpain activation trigger muscle proteolysis and atrophy while protein synthesis is impaired. Myosin loss is more pronounced than actin loss in CIM. Protein quality control is altered by inadequate autophagy. Ca2+dysregulation is present through altered Ca2+homeostasis. We highlight clinical hallmarks, trigger factors, and potential mechanisms from human studies and animal models that allow separation of risk factors that may trigger distinct mechanisms contributing to weakness. During critical illness, altered inflammatory (cytokines) and metabolic pathways deteriorate muscle function. ICUAW prevention/treatment is limited, e.g., tight glycemic control, delaying nutrition, and early mobilization. Future challenges include identification of primary/secondary events during the time course of critical illness, the interplay between membrane excitability, bioenergetic failure and differential proteolysis, and finding new therapeutic targets by help of tailored animal models.

O-GlcNAc transferase inhibitors: current tools and future challenges

2016 ◽  
Vol 44 (1) ◽  
pp. 88-93 ◽  
Author(s):  
Riccardo Trapannone ◽  
Karim Rafie ◽  
Daan M.F. van Aalten
Keyword(s):  
Animal Models ◽  
Biological Systems ◽  
Biological Role ◽  
Present Review ◽  
Biological Functions ◽  
Post Translational Modification ◽  
Embryonic Lethal ◽  
Future Challenges ◽  
Glcnac Transferase

The O-linked N-acetylglucosamine (O-GlcNAc) post-translational modification (O-GlcNAcylation) is the dynamic and reversible attachment of N-acetylglucosamine to serine and threonine residues of nucleocytoplasmic target proteins. It is abundant in metazoa, involving hundreds of proteins linked to a plethora of biological functions with implications in human diseases. The process is catalysed by two enzymes: O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA) that add and remove sugar moieties respectively. OGT knockout is embryonic lethal in a range of animal models, hampering the study of the biological role of O-GlcNAc and the dissection of catalytic compared with non-catalytic roles of OGT. Therefore, selective and potent chemical tools are necessary to inhibit OGT activity in the context of biological systems. The present review focuses on the available OGT inhibitors and summarizes advantages, limitations and future challenges.

Evaluation of biotechnology-derived novel proteins for the risk of food-allergic potential: advances in the development of animal models and future challenges

2010 ◽  
Vol 84 (12) ◽  
pp. 909-917 ◽  
Author(s):  
Varun Ahuja ◽  
Maria Quatchadze ◽  
Vaishali Ahuja ◽  
Daniela Stelter ◽  
Achim Albrecht ◽  
...  
Keyword(s):  
Animal Models ◽  
Novel Proteins ◽  
Future Challenges

scholarly journals Animal models of major depression: drawbacks and challenges

2019 ◽  
Vol 126 (11) ◽  
pp. 1383-1408 ◽  
Author(s):  
Barbara Planchez ◽  
Alexandre Surget ◽  
Catherine Belzung
Keyword(s):  
Major Depression ◽  
Animal Models ◽  
Poor Response ◽  
Treatment Resistant Depression ◽  
Recurrent Depression ◽  
Treatment Resistant ◽  
Neuronal Populations ◽  
Future Challenges ◽  
Resistant Depression ◽  
Depression Subtypes

Abstract Major depression is a leading contributor to the global burden of disease. This situation is mainly related to the chronicity and/or recurrence of the disorder, and to poor response to antidepressant therapy. Progress in this area requires valid animal models. Current models are based either on manipulating the environment to which rodents are exposed (during the developmental period or adulthood) or biological underpinnings (i.e. gene deletion or overexpression of candidate genes, targeted lesions of brain areas, optogenetic control of specific neuronal populations, etc.). These manipulations can alter specific behavioural and biological outcomes that can be related to different symptomatic and pathophysiological dimensions of major depression. However, animal models of major depression display substantial shortcomings that contribute to the lack of innovative pharmacological approaches in recent decades and which hamper our capabilities to investigate treatment-resistant depression. Here, we discuss the validity of these models, review putative models of treatment-resistant depression, major depression subtypes and recurrent depression. Furthermore, we identify future challenges regarding new paradigms such as those proposing dimensional rather than categorical approaches to depression.

scholarly journals Intracerebral haemorrhage: from clinical settings to animal models

2020 ◽  
Vol 5 (4) ◽  
pp. 388-395
Author(s):  
Qian Bai ◽  
Zhaofu Sheng ◽  
Yang Liu ◽  
Ruiyi Zhang ◽  
Voon Wee Yong ◽  
...  
Keyword(s):  
Animal Models ◽  
Clinical Research ◽  
High Mortality ◽  
Intracerebral Haemorrhage ◽  
Therapeutic Strategies ◽  
Clinical Settings ◽  
Mortality And Morbidity ◽  
Inflammatory Cascade ◽  
Future Challenges ◽  
Spontaneous Intracerebral Haemorrhage

Spontaneous intracerebral haemorrhage (ICH) is a devastating type of stroke with high mortality and morbidity and for which no effective treatments are available to date. Much experimental and clinical research have been performed to explore its mechanisms regard the subsequent inflammatory cascade and to seek the potential therapeutic strategies. The aim of this review is to discuss insights from clinical settings that have led to the development of numerous animal models of ICH. Some of the current and future challenges for clinicians to understand ICH are also surveyed.

scholarly journals Animal Models of Typical Heterotopic Ossification

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Lixin Kan ◽  
John A. Kessler
Keyword(s):  
Animal Models ◽  
Heterotopic Ossification ◽  
Traumatic Events ◽  
Limiting Factor ◽  
Clinical Complication ◽  
Future Challenges ◽  
Life Threatening ◽  
Substantial Effort

Heterotopic ossification (HO) is the formation of marrow-containing bone outside of the normal skeleton. Acquired HO following traumatic events is a common and costly clinical complication. In contrast, hereditary HO is rarer, progressive, and life-threatening. Substantial effort has been directed towards understanding the mechanisms underlying HO and finding efficient treatments. However, one crucial limiting factor has been the lack of relevant animal models. This article reviews the major currently available animal models, summarizes some of the insights gained from these studies, and discusses the potential future challenges and directions in HO research.

Brain Reward Circuits in Alcoholism

CNS Spectrums ◽  
1999 ◽  
Vol 4 (1) ◽  
pp. 23-37 ◽  
Author(s):  
George F. Koob ◽  
Amanda J. Roberts
Keyword(s):  
Animal Models ◽  
Positive Reinforcement ◽  
Negative Reinforcement ◽  
Behavioral Disorder ◽  
Behavioral Repertoire ◽  
Neuronal Membranes ◽  
Future Challenges ◽  
History Of ◽  
Excessive Consumption ◽  
Set Up

AbstractThis article discusses the neurocircuitry and the neurochemical systems, as well as the molecular elements within these systems, that are believed to be important in the etiology of alcoholism. Alcoholism is a complex behavioral disorder characterized by excessive consumption of alcohol; a narrowing of the behavioral repertoire toward excessive consumption; the development of tolerance and dependence; and impairment in social and occupational functioning. Animal models of the complete syndrome of alcoholism are difficult if not impossible to achieve, but validated animal models exist for many of the different components of the syndrome.Recent work has begun to define the neurocircuits responsible for the major sources of positive and negative reinforcement that are key to animal models of excessive alcohol intake. Alcohol appears to interact with alcohol-sensitive elements within neuronal membranes that convey the specificity of neurochemical actions. Positive reinforcement appears to be mediated by an activation γ-aminobutyric acid A receptors, release of opioid peptides and dopamine, inhibition of glutamate receptors, and interaction with serotonin systems. These neurocircuits may be altered by chronic alcohol administration. This is reflected by their exhibiting opposite effects during acute alcohol withdrawal, and by the recruitment of other neurotransmitter systems, such as the stress neuropeptide corticotropin-releasing factor. These neuropharmacologic actions are believed to produce allostatic changes in set-point, which set up the vulnerability to relapse that is so characteristic of alcoholism. Future challenges include a focus on understanding exactly how these neuroadaptive changes convey vulnerability to relapse in animals with a history of alcohol dependence.

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