Coxsackievirus Cardiomyopathy in Animal Models, Including the Augmenting Effect of Exercise During the Acute Phase

1988 ◽  
pp. 61-69
Author(s):  
M. P. Reyes ◽  
A. M. Lerner ◽  
R. Khatib
Keyword(s):  
Animal Models ◽  
Acute Phase

scholarly journals Targeted Delivery of Plasminogen Activators for Thrombolytic Therapy: An Integrative Evaluation

Molecules ◽  
2019 ◽  
Vol 24 (18) ◽  
pp. 3407 ◽  
Author(s):  
Yunn-Hwa Ma ◽  
Chih-Hsin Liu ◽  
Yueh Liang ◽  
Jyh-Ping Chen ◽  
Tony Wu
Keyword(s):  
Animal Models ◽  
Thrombolytic Therapy ◽  
Surface Properties ◽  
Acute Phase ◽  
Targeted Delivery ◽  
Therapeutic Efficacy ◽  
Recent Progress ◽  
Plasminogen Activators ◽  
Integrative Evaluation

In thrombolytic therapy, plasminogen activators (PAs) are still the only group of drug approved to induce thrombolysis, and therefore, critical for treatment of arterial thromboembolism, such as stroke, in the acute phase. Functionalized nanocomposites have attracted great attention in achieving target thrombolysis due to favorable characteristics associated with the size, surface properties and targeting effects. Many PA-conjugated nanocomposites have been prepared and characterized, and some of them has been demonstrated with therapeutic efficacy in animal models. To facilitate future translation, this paper reviews recent progress of this area, especially focus on how to achieve reproducible thrombolysis efficacy in vivo.

Abstract 465: Lipid-lowering Agent Gemcabene Down-regulates Acute Phase C-reactiveProtein via /EBP-δ-mediated Transcriptional Mechanism and Attenuates Inflammation and Osteoarthritis in Animal Models

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Rai Ajit K Srivastava ◽  
Joseph A Cornicelli ◽  
Bruce E Markham ◽  
Charles L Bisgaier
Keyword(s):  
Animal Models ◽  
Acute Phase ◽  
Binding Sites ◽  
Lipid Lowering ◽  
Hepatoma Cell Line ◽  
Regulatory Sequences ◽  
Dependent Manner ◽  
Down Regulation ◽  
Anti Inflammatory ◽  
Dose Dependent

Background: Inflammation plays a key role in setting the stage as well as causing the progression of atherosclerosis. High sensitivity c-reactive protein (hsCRP), an acute phase reactant released during inflammatory processes, has been recognized as a predictor of cardiovascular risk. Experiments & Results: Since gemcabene reduced hsCRP in humans, we investigated the mechanism of hsCRP reduction and efficacy of anti-inflammatory activity in animal models of arthritis and pain. In human hepatoma cell line, PLC/PRF/5, gemcabene showed dose-dependent inhibition of IL-6+ IL-1β-induced CRP production by -70% inhibition at 2 mM. In TNF-α-stimulated primary human coronary artery endothelial cells, both CRP and IL-6 productions were inhibited by gemcabene in a dose-dependent manner (-70% at 2mM). Transfection studies with human CRP regulatory sequences in luciferase/ β-gal system showed a 25-fold increase in IL-6- as well as IL-6+ IL-1β -stimulated CRP transcription, which was reduced by gemcabene (-50% at 2 mM), suggesting transcriptional down-regulation of CRP. Site-directed mutation of C/EBP, NF-κB, and STAT sites of the human CRP promoter suggested that the overlapping downstream C/EBP and NF-κB binding sites are important for gemcabene-mediated down-regulation of CRP promoter. STAT3 response element, while needed for IL-6-induced expression of CRP, is not required for gemcabene-mediated inhibition. Identification of the protein, in a gel-shift assay, that interacts with C/EBP binding sites revealed it to be C/EBPδ. Anti-inflammatory efficacy of gemcabene was evaluated in a rat model of monosodium iodoacetate (MIA)-induced osteoarthritis (OA) and carrageenan-induced thermal hyperalgesia (CITH). Gemcabene improved joint comfort (-50% at 30 mg/kg/d for 2 wk) in MIA and attenuated paw withdrawal latency (60% at 30 mg/kg/d and 97% at 100 mg/kg/d, compared to untreated control) in the CITH model. These findings were further confirmed by an IL-6/IL-6sR knee injection model showing 63 and 71% reduction in hind paw weight distribution at 10 and 30 mg/kg/d doses, respectively. Conclusions: Gemcabene decreases CRP by C/EBPδ and NF-κB mediated transcriptional mechanism, and attenuates inflammation-induced OA and hyperalgesia.

Reductionist thinking and animal models in neuropsychiatric research

2019 ◽  
Vol 42 ◽  
Author(s):  
Nicole M. Baran
Keyword(s):  
Animal Models ◽  
Mental Disorders ◽  
Environmental Factors ◽  
Neuropsychiatric Disorders ◽  
Model Organisms ◽  
Developmental Genetic ◽  
Term Study ◽  
Genetic And Environmental Factors ◽  
Mechanisms Of Plasticity

AbstractReductionist thinking in neuroscience is manifest in the widespread use of animal models of neuropsychiatric disorders. Broader investigations of diverse behaviors in non-model organisms and longer-term study of the mechanisms of plasticity will yield fundamental insights into the neurobiological, developmental, genetic, and environmental factors contributing to the “massively multifactorial system networks” which go awry in mental disorders.

Inflammational Animal Models for Schizophrenia

2015 ◽  
Vol 223 (3) ◽  
pp. 157-164 ◽  
Author(s):  
Georg Juckel
Keyword(s):  
Animal Model ◽  
Animal Models ◽  
Immune Activation ◽  
Microglial Activation ◽  
Treatment Options ◽  
Early Adulthood ◽  
Brain Regions ◽  
Synaptic Connections ◽  
Preventive Interventions ◽  
Immunological System

Abstract. Inflammational-immunological processes within the pathophysiology of schizophrenia seem to play an important role. Early signals of neurobiological changes in the embryonal phase of brain in later patients with schizophrenia might lead to activation of the immunological system, for example, of cytokines and microglial cells. Microglia then induces – via the neurotoxic activities of these cells as an overreaction – a rarification of synaptic connections in frontal and temporal brain regions, that is, reduction of the neuropil. Promising inflammational animal models for schizophrenia with high validity can be used today to mimic behavioral as well as neurobiological findings in patients, for example, the well-known neurochemical alterations of dopaminergic, glutamatergic, serotonergic, and other neurotransmitter systems. Also the microglial activation can be modeled well within one of this models, that is, the inflammational PolyI:C animal model of schizophrenia, showing a time peak in late adolescence/early adulthood. The exact mechanism, by which activated microglia cells then triggers further neurodegeneration, must now be investigated in broader detail. Thus, these animal models can be used to understand the pathophysiology of schizophrenia better especially concerning the interaction of immune activation, inflammation, and neurodegeneration. This could also lead to the development of anti-inflammational treatment options and of preventive interventions.

Animal models of psychopathology: The low-norepinephrine and low-serotonin rat.

1977 ◽  
Vol 32 (12) ◽  
pp. 1036-1045 ◽  
Author(s):  
Gaylord D. Ellison
Keyword(s):  
Animal Models

Sex difference in depression: Which animal models mimic it.

2020 ◽  
Vol 134 (3) ◽  
pp. 248-266
Author(s):  
Javed Iqbal ◽  
Frank Adu-Nti ◽  
Xuejiao Wang ◽  
Hui Qiao ◽  
Xin-Ming Ma
Keyword(s):  
Animal Models ◽  
Sex Difference
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