The Development and Use of Animal Models in Atherosclerosis Research

1987 ◽  
pp. 337-357 ◽  
Author(s):  
Robert W. Wissler ◽  
Dragoslava Vesselinovitch
Keyword(s):  
Animal Models ◽  
Atherosclerosis Research

scholarly journals Animal models for the atherosclerosis research: a review

2011 ◽  
Vol 2 (3) ◽  
pp. 189-201 ◽  
Author(s):  
Li Xiangdong ◽  
Liu Yuanwu ◽  
Zhang Hua ◽  
Ren Liming ◽  
Li Qiuyan ◽  
...  
Keyword(s):  
Animal Models ◽  
Atherosclerosis Research

Animal models of spontaneous plaque rupture: The holy grail of experimental atherosclerosis research

2002 ◽  
Vol 4 (3) ◽  
pp. 238-242 ◽  
Author(s):  
Michael E. Rosenfeld ◽  
Kevin G. S. Carson ◽  
Jason L. Johnson ◽  
Helen Williams ◽  
Christopher L. Jackson ◽  
...  
Keyword(s):  
Animal Models ◽  
Plaque Rupture ◽  
Experimental Atherosclerosis ◽  
Holy Grail ◽  
Atherosclerosis Research

Electrical Aggregometry in Whole Blood from Human, Pig and Rabbit

1986 ◽  
Vol 56 (02) ◽  
pp. 128-132 ◽  
Author(s):  
Angel E Galvez ◽  
Lina Badimon ◽  
Juan-Jose Badimon ◽  
Valentin Fuster
Keyword(s):  
Platelet Aggregation ◽  
Animal Models ◽  
Dose Response ◽  
Whole Blood ◽  
Platelet Rich Plasma ◽  
Platelet Response ◽  
Response Curves ◽  
Rabbit Platelets ◽  
Atherosclerosis Research ◽  
Research Animal

SummaryThe objective of this study was to characterize and standardize whole blood electrical aggregometry (WBEA) in the pig and rabbit, animal models extensively used in atherosclerosis research, and to compare their platelet response with that of man. Platelet aggregation was studied in blood (WBEA) and platelet rich plasma (optical aggregometry, OA). Dose response curves were obtained for ADP and collagen. The effect of hematocrit on WBEA was also evaluated. Aggregation with ADP and collagen using WBEA was more extensive with human than with pig or rabbit platelets. OA revealed similar differences among species but the time to reach maximal aggregation was markedly shorter. Using WBEA, the extent of aggregation was inversely related to the hematocrit. We conclude that WBEA is a useful technique that may be of particular importance in situations where hyper-lipidemic plasma prevents the use of OA, as occurs in some atherosclerosis research animal models.

Spider monkeys (Ateles sp.) as animal models for atherosclerosis research

1973 ◽  
Vol 18 (1) ◽  
pp. 32-49 ◽  
Author(s):  
G.J. Pucak ◽  
N.D.M. Lehner ◽  
T.B. Clarkson ◽  
B.C. Bullock ◽  
H.B. Lofland
Keyword(s):  
Animal Models ◽  
Spider Monkeys ◽  
Atherosclerosis Research

An update of the contributions of animal models to atherosclerosis research

1994 ◽  
Vol 109 (1-2) ◽  
pp. 9
Author(s):  
D. Vesselinovitch ◽  
R.W. Wissler
Keyword(s):  
Animal Models ◽  
Atherosclerosis Research

Animal models in atherosclerosis research

1985 ◽  
Vol 42 (1) ◽  
pp. 1-28 ◽  
Author(s):  
Micheal P. Jokinen ◽  
Thomas B. Clarkson ◽  
Robert W. Prichard
Keyword(s):  
Animal Models ◽  
Atherosclerosis Research

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.

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