Compression-Induced Tissue Damage: Animal Models

2005 ◽  
pp. 187-204 ◽  
Author(s):  
Anke Stekelenburg ◽  
Cees Oomens ◽  
Dan Bader
Keyword(s):  
Animal Models ◽  
Tissue Damage

Characterization of white matter damage in animal models of multiple sclerosis by magnetization transfer ratio and quantitative mapping of the apparent bound proton fraction f*

2009 ◽  
Vol 15 (1) ◽  
pp. 16-27 ◽  
Author(s):  
M Rausch ◽  
PS Tofts ◽  
P Lervik ◽  
AR Walmsley ◽  
A Mir ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
White Matter ◽  
Animal Models ◽  
Tissue Damage ◽  
Magnetization Transfer ◽  
Transverse Relaxation Time ◽  
Magnetization Transfer Ratio ◽  
White Matter Damage ◽  
Transfer Ratio ◽  
Quantitative Mapping

Quantitative magnetization transfer magnetic resonance imaging (qMT-MRI) can be used to improve detection of white matter tissue damage in multiple sclerosis (MS) and animal models thereof. To study the correlation between MT parameters and tissue damage, the magnetization transfer ratio (MTR), the parameter f* (closely related to the bound proton fraction) and the bound proton transverse relaxation time T2B of lesions in a model of focal experimental autoimmune encephalomyelitis (EAE) were measured on a 7T animal scanner and data were compared with histological markers indicative for demyelination, axonal density, and tissue damage. A clear spatial correspondence was observed between reduced values of MTR and demyelination in this animal model. We observed two different levels of MTR and f* reduction for these lesions. One was characterized by a pronounced demyelination and the other corresponded to a more severe loss of the cellular matrix. Changes in f* were generally more pronounced than those of MTR in areas of demyelination. Moreover, a reduction of f* was already observed for tissue where MTR was virtually normal. No changes in T2B were observed for the lesions. We conclude that MTR and qMT mapping are efficient and reliable readouts for studying demyelination in animal models of MS, and that the analysis of regional f* might be even superior to the analysis of MTR values. Therefore, quantitative mapping of f* from human brains might also improve the detection of white matter damage in MS.

scholarly journals MRI to predict severe tissue damage in inflammatory lesions in animal models of multiple sclerosis

Brain ◽  
2008 ◽  
Vol 131 (3) ◽  
pp. e92-e92 ◽  
Author(s):  
B. Brochet ◽  
V. Dousset ◽  
M. Deloire ◽  
C. Boiziau ◽  
K. G. Petry
Keyword(s):  
Multiple Sclerosis ◽  
Animal Models ◽  
Tissue Damage ◽  
Inflammatory Lesions ◽  
Severe Tissue

The challenges of animal models of pain

2018 ◽  
Author(s):  
Muhammad Saad Yousuf ◽  
Bradley J. Kerr
Keyword(s):  
Animal Models ◽  
Tissue Damage ◽  
Emotional Experience ◽  
Human Studies ◽  
Common Symptom ◽  
Biological Mechanisms ◽  
Ethical Considerations ◽  
Physician Consultation ◽  
Mcgill University ◽  
Unpleasant Feeling

The landmark paper discussed in this chapter is ‘Animal models of pain: progress and challenges’, published in the journal Nature Reviews Neuroscience by Jeff Mogil of McGill University in 2009. The most common symptom across various medical conditions and a major reason for seeking physician consultation is pain. It is defined as ‘an unpleasant feeling or emotional experience associated with actual or potential tissue damage’. A large percentage of the research investigating the biological mechanisms of pain is performed on animals. Human studies of pain are limited by lack of practicality, subjectivity, and ethical considerations. This influential review by Mogil discusses the progress and challenges faced in studying pain using various animal models.

scholarly journals In vivo animal models confirm an increased virulence potential and pathogenicity of the NAP1/RT027/ST01 genotype within the Clostridium difficile MLST Clade 2

Gut Pathogens ◽  
2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Josué Orozco-Aguilar ◽  
Alejandro Alfaro-Alarcón ◽  
Luis Acuña-Amador ◽  
Esteban Chaves-Olarte ◽  
César Rodríguez ◽  
...  
Keyword(s):  
Animal Models ◽  
Tissue Damage ◽  
Animal Experiments ◽  
Histological Evaluation ◽  
Loop Model ◽  
Ileal Loop ◽  
Pathogenic Potential ◽  
Virulence Potential ◽  
Sequence Types

Abstract Background Based on MLST analyses the global population of C. difficile is distributed in eight clades, of which Clade 2 includes the “hypervirulent” NAP1/RT027/ST01 strain along with various unexplored sequence types (STs). Methods To clarify whether this clinically relevant phenotype is a widespread feature of C. difficile Clade 2, we used the murine ileal loop model to compare the in vivo pro-inflammatory (TNF-α, IL-1β, IL-6) and oxidative stress activities (MPO) of five Clade 2 clinical C. difficile isolates from sequence types (STs) 01, 41, 67, and 252. Besides, we infected Golden Syrian hamsters with spores from these strains to determine their lethality, and obtain a histological evaluation of tissue damage, WBC counts, and serum injury biomarkers (LDH, ALT, AST, albumin, BUN, creatinine, Na+, and Cl−). Genomic distances were calculated using Mash and FastANI to explore whether the responses were dictated by phylogeny. Results The ST01 isolate tested ranked first in all assays, as it induced the highest overall levels of pro-inflammatory cytokines, MPO activity, epithelial damage, biochemical markers, and mortality measured in both animal models. Statistically indistinguishable or rather similar outputs were obtained for a ST67 isolate in tests such as tissue damage, neutrophils count, and lethal activity. The results recorded for the two ST41 isolates tested were of intermediate magnitude and the ST252 isolate displayed the lowest pathogenic potential in all animal experiments. This ordering matched the genomic distance of the ST01 isolate to the non-ST01 isolates. Conclusions Despite their close phylogenic relatedness, our results demonstrate differences in pathogenicity and virulence levels in Clade 2 C. difficile strains, confirm the high severity of infections caused by the NAP1/RT027/ST01 strain, and highlight the importance of C. difficile typing.

scholarly journals The specificity of thiourea, dimethylthiourea and dimethyl sulphoxide as scavengers of hydroxyl radicals. Their protection of α1-antiproteinase against inactivation by hypochlorous acid

1987 ◽  
Vol 243 (3) ◽  
pp. 867-870 ◽  
Author(s):  
M Wasil ◽  
B Halliwell ◽  
M Grootveld ◽  
C P Moorhouse ◽  
D C S Hutchison ◽  
...  
Keyword(s):  
Animal Models ◽  
Hydroxyl Radicals ◽  
Tissue Damage ◽  
Human Disease ◽  
Hypochlorous Acid ◽  
Dimethyl Sulphoxide

Thiourea and dimethylthiourea are powerful scavengers of hydroxyl radicals (.OH), and dimethylthiourea has been used to test the involvement of .OH in several animal models of human disease. It is shown that both thiourea and dimethylthiourea are scavengers of HOCl, a powerful oxidant produced by neutrophil myeloperoxidase. Hence the ability of dimethylthiourea to protect against neutrophil-mediated tissue damage cannot be used as evidence for a role of .OH in causing such damage. Dimethyl sulphoxide also reacts with HOCl, but at a rate that is probably too low to be biologically significant at dimethyl sulphoxide concentrations up to 10 mM. Neither mannitol nor desferrioxamine, at the concentrations normally used in radical-generating systems, appears to react with HOCl.

scholarly journals Sliding set-points of immune responses for therapy of autoimmunity

2010 ◽  
Vol 207 (9) ◽  
pp. 1819-1823 ◽  
Author(s):  
Chyi-Song Hsieh ◽  
Jhoanne Lynne Bautista
Keyword(s):  
T Cells ◽  
Autoimmune Disease ◽  
Animal Models ◽  
Immune Responses ◽  
Patient Outcomes ◽  
Tissue Damage ◽  
The Body ◽  
Short Term ◽  
Self Tolerance ◽  
Recent Developments

Although recent developments in the treatment of autoimmune disease have dramatically improved patient outcomes, these medications are not curative. Two studies in this issue demonstrate the feasibility of curing spontaneous autoimmunity in animal models via short-term enhancement of naturally arising regulatory T (T reg) cells, a subset of CD4+ T cells needed for maintaining self-tolerance. Importantly, these therapies seemed to generate a new equilibrium, or “set-point,” at which self-tissue damage no longer occurred long after the drug was eliminated from the body.

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.

Artifacts caused by dehydration and epoxy embedding in TEM

1991 ◽  
Vol 49 ◽  
pp. 338-339
Author(s):  
Hilton H. Mollenhauer
Keyword(s):  
Electron Microscopy ◽  
Electron Beam ◽  
Volume Change ◽  
Tissue Damage ◽  
Beam Specimen ◽  
Chemical Fixation ◽  
Resin Impregnation ◽  
Storage Vesicles ◽  
A Cell ◽  
Tissue Shrinkage

Various means have been devised to preserve biological specimens for electron microscopy, the most common being chemical fixation followed by dehydration and resin impregnation. It is intuitive, and has been amply demonstrated, that these manipulations lead to aberrations of many tissue elements. This report deals with three parts of this problem: specimen dehydration, epoxy embedding resins, and electron beam-specimen interactions. However, because of limited space, only a few points can be summarized.Dehydration: Tissue damage, or at least some molecular transitions within the tissue, must occur during passage of a cell or tissue to a nonaqueous state. Most obvious, perhaps, is a loss of lipid, both that which is in the form of storage vesicles and that associated with tissue elements, particularly membranes. Loss of water during dehydration may also lead to tissue shrinkage of 5-70% (volume change) depending on the tissue and dehydrating agent.

Ultrastructure and analytical microprobe analysis of simian lung mite pigments

1986 ◽  
Vol 44 ◽  
pp. 324-325
Author(s):  
R. W. Cole ◽  
J. C. Kim
Keyword(s):  
Biomedical Research ◽  
Tissue Damage ◽  
Microprobe Analysis ◽  
Old World Monkeys ◽  
Old World ◽  
Experimental Animals ◽  
The Past ◽  
Lung Mite ◽  
Mite Infestations ◽  
Cardiopulmonary System

In recent years, non-human primates have become indispensable as experimental animals in many fields of biomedical research. Pharmaceutical and related industries alone use about 2000,000 primates a year. Respiratory mite infestations in lungs of old world monkeys are of particular concern because the resulting tissue damage can directly effect experimental results, especially in those studies involving the cardiopulmonary system. There has been increasing documentation of primate parasitology in the past twenty years.

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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