Preparation of an Antiserum Specific to a Spontaneous Mouse Leukæmia after the Induction of Artificial Immunological Tolerance to Normal Mouse Tissue

Nature ◽  
1963 ◽  
Vol 199 (4892) ◽  
pp. 501-502 ◽  
Author(s):  
ELAINE LEVI
Keyword(s):  
Normal Mouse ◽  
Immunological Tolerance ◽  
Mouse Tissue ◽  
Mouse Leukaemia

scholarly journals Localization of urokinase-type plasminogen activator messenger RNA in the normal mouse by in situ hybridization.

1991 ◽  
Vol 39 (3) ◽  
pp. 341-349 ◽  
Author(s):  
P Kristensen ◽  
J Eriksen ◽  
K Danø
Keyword(s):  
In Situ Hybridization ◽  
Plasminogen Activator ◽  
Normal Mouse ◽  
Hybridization Signal ◽  
Mouse Tissue ◽  
Northern Analysis ◽  
Type Plasminogen Activator ◽  
Urokinase Type Plasminogen Activator ◽  
Collecting Tubules

The histological distribution of urokinase-type plasminogen activator (u-PA) mRNA was analyzed in normal mouse tissue by in situ hybridization with anti-sense RNA transcribed from three different subclones of a mouse u-PA cDNA. Hybridization signal was found over a distinct fibroblast-like cell in the lamina propria of the gastrointestinal tract, over proximal, distal, and collecting tubules of the kidney, and over the epithelium of the bladder, ductus deferens, and epididymis. No hybridization signal was found over cells of the lung, pancreas, liver, adrenal, pituitary, cerebrum, hypothalamus, cerebellum, sciatic nerve, and striated muscle, nor over endothelial cells in any tissue investigated. The lack of u-PA mRNA in lung tissue was confirmed by Northern analysis and is in contrast to the high amounts of u-PA protein found in this tissue.

Irradiation of normal mouse tissue increases the invasiveness of mammary cancer cells

2011 ◽  
Vol 87 (5) ◽  
pp. 472-482 ◽  
Author(s):  
Rosalie Lemay ◽  
Mélanie Archambault ◽  
Luc Tremblay ◽  
Rachel Bujold ◽  
Martin Lepage ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Mammary Cancer ◽  
Normal Mouse ◽  
Mouse Tissue ◽  
Mammary Cancer Cells

LYMPHOCYTIC CHORIOMENINGITIS INFECTION OF MICE AS A MODEL FOR THE STUDY OF LATENT VIRUS INFECTION

1958 ◽  
Vol 4 (2) ◽  
pp. 149-163 ◽  
Author(s):  
J. E. Hotchin ◽  
M. Cinits
Keyword(s):  
Virus Infection ◽  
Immunological Tolerance ◽  
Lymphocytic Choriomeningitis ◽  
Latent Virus ◽  
Mouse Tissue ◽  
Virus Infections ◽  
Latently Infected ◽  
Set Up ◽  
Cytopathogenic Effect

Lymphocytic choriomeningitis virus has been used to set up a model of a latent virus infection in mice. It has been shown to be possible to induce reproducible virus infections in mice which remain completely symptom-free in spite of levels of viral growth equal to those found in the sick animal, by the inoculation of mice within a few hours of birth. This is a convenient method of producing a latent infection in the mice. The effect of the age of the mice at the time of intracerebral inoculation was studied with respect to the pattern of disease produced. Several methods were tried without success in order to induce overt disease in the latently infected animals. The virus did not cause any demonstrable cytopathogenic effect on mouse tissue and several other types of animal tissue. A slight cytopathogenic effect was observed in a strain of human cells in vitro. Virus persisted for weeks in some of the tissue cultures, without damaging the tissue but with the production of active virus. The bearing of the results obtained is discussed in relationship to current concepts of latent virus infection and particularly immunological tolerance. A concept of a special variety of latency is introduced and the name "vital" infection suggested for this.

scholarly journals Heart-specific autoantibodies following murine coxsackievirus B3 myocarditis.

1985 ◽  
Vol 161 (5) ◽  
pp. 1112-1121 ◽  
Author(s):  
L J Wolfgram ◽  
K W Beisel ◽  
N R Rose
Keyword(s):  
Skeletal Muscle ◽  
Animal Model ◽  
Indirect Immunofluorescence ◽  
Normal Mouse ◽  
Viral Myocarditis ◽  
Coxsackievirus B3 ◽  
Autoimmune Response ◽  
Mouse Tissue ◽  
Absorption Studies

The sera from A.SW/SnJ mice infected with Coxsackievirus B3 (CB3) were tested on normal mouse tissue by indirect immunofluorescence. Heart-reactive antibodies were found. Absorption studies with organ extracts showed some of these autoantibodies to be heart-specific. Additional antibodies were crossreactive with skeletal muscle and kidney. These findings suggest a role for autoimmunity in the pathogenesis of murine CB3-induced myocarditis. This study establishes an animal model for the study of the humoral autoimmune response in human viral myocarditis.

Hydrocarbon carcinogens induce p53 activity in normal mouse tissue

2001 ◽  
Vol 173 (2) ◽  
pp. 111-114 ◽  
Author(s):  
D Stuart ◽  
Q.A Khan ◽  
R Brown ◽  
A Dipple
Keyword(s):  
Normal Mouse ◽  
Mouse Tissue

Molecular and Microscopic Analysis of Altered Gene Expression in Transgenic and Gene Targeted Mice

1996 ◽  
Vol 54 ◽  
pp. 12-13
Author(s):  
W. K. Jones ◽  
J. Robbins
Keyword(s):  
Gene Expression ◽  
Pulmonary Veins ◽  
Microscopic Analysis ◽  
Mouse Tissue ◽  
Adult Heart ◽  
Heavy Chains ◽  
Altered Gene Expression ◽  
Altered Gene ◽  
Pulmonary Myocardium

Two myosin heavy chains (MyHC) are expressed in the mammalian heart and are differentially regulated during development. In the mouse, the α-MyHC is expressed constitutively in the atrium. At birth, the β-MyHC is downregulated and replaced by the α-MyHC, which is the sole cardiac MyHC isoform in the adult heart. We have employed transgenic and gene-targeting methodologies to study the regulation of cardiac MyHC gene expression and the functional and developmental consequences of altered α-MyHC expression in the mouse.We previously characterized an α-MyHC promoter capable of driving tissue-specific and developmentally correct expression of a CAT (chloramphenicol acetyltransferase) marker in the mouse. Tissue surveys detected a small amount of CAT activity in the lung (Fig. 1a). The results of in situ hybridization analyses indicated that the pattern of CAT transcript in the adult heart (Fig. 1b, top panel) is the same as that of α-MyHC (Fig. 1b, lower panel). The α-MyHC gene is expressed in a layer of cardiac muscle (pulmonary myocardium) associated with the pulmonary veins (Fig. 1c). These studies extend our understanding of α-MyHC expression and delimit a third cardiac compartment.

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