scholarly journals AN ANIMAL MODEL FOR ESTABLISHING CHEMOTHERAPY AGAINST INTRACTABLE TOXOPLASMOSIS IN IMMUNOCOMPROMISED HOSTS BY THE USE OF IFN-.GAMMA. KNOCKOUT MICE.

2003 ◽  
Vol 31 (2) ◽  
pp. 83-86
Author(s):  
USAMA S. BELAL ◽  
KAZUMI NOROSE ◽  
HYE-SEONG MUN ◽  
MEI CHEN ◽  
RABIE M. MOHAMED ◽  
...  
Keyword(s):  
Animal Model ◽  
Knockout Mice ◽  
Ifn Gamma ◽  
Immunocompromised Hosts

Knockout Mice Offer First Animal Model for CF

Science ◽  
1992 ◽  
Vol 257 (5073) ◽  
pp. 1046-1047 ◽  
Author(s):  
M. Barinaga
Keyword(s):  
Animal Model ◽  
Knockout Mice

scholarly journals Alterations of Amino Acids and Monoamine Metabolism in Male Fmr1 Knockout Mice: A Putative Animal Model of the Human Fragile X Mental Retardation Syndrome

2001 ◽  
Vol 8 (4) ◽  
pp. 285-298 ◽  
Author(s):  
Michael Gruss ◽  
Katharina Braun
Keyword(s):  
Amino Acids ◽  
Animal Model ◽  
Mental Retardation ◽  
Fragile X Syndrome ◽  
Knockout Mice ◽  
Fragile X ◽  
Fragile X Mental Retardation ◽  
Behavioral Abnormalities ◽  
Cortical Regions ◽  
Knockout Animals

The Fragile X syndrome, a common form of mental retardation in humans, is caused by silencing the fragile X mental retardation (FMR1) geneleading to the absence of the encoded fragile X mental retardation protein 1 (FMRP). We describe morphological and behavioral abnormalities for both affected humans and Fmr1 knockout mice, a putative animal model for the human Fragile X syndrome. The aim of the present study was to identify possible neurochemical abnormalities in Fmr1 knockout mice, with particular focus on neurotransmission. Significant region-specific differences: of basal neurotransmitter and metabolite levels were found between wildtype and Fmr1 knockout animals, predominantly in juveniles (post-natal days 28 to 31). Adults (postnatal days 209 to 221) showed only few abnormalities as compared with the wildtype. In juvenile knockout mice, aspartate and taurine were especially increased in cortical regions, striatum, hippocampus, cerebellum, and brainstem. In addition, juveniles showed an altered balance between excitatory and inhibitory amino acids in the caudal cortex, hippocampus, and brainstem. We detected very few differences in monoamine turnover in both age stages. The results presented here provide the first evidence that lack of FMRP expression in FMRP knockout mice is accompanied by age-dependent, region-specific alterations in neurotransmission.

4.P.362 Lecithin: Cholesterol acyltransferase (LCAT) knockout mice: A new animal model for human LCAT-deficiency

1997 ◽  
Vol 134 (1-2) ◽  
pp. 372-373
Author(s):  
N. Sakai ◽  
B.L. Vaisman ◽  
C.A. Koch ◽  
R.F. Hoyt ◽  
S.M. Meyn ◽  
...  
Keyword(s):  
Animal Model ◽  
Knockout Mice ◽  
Cholesterol Acyltransferase ◽  
Lecithin Cholesterol Acyltransferase ◽  
Lcat Deficiency

scholarly journals CD4+ effector cells default to the Th2 pathway in interferon gamma-deficient mice infected with Leishmania major.

1994 ◽  
Vol 179 (4) ◽  
pp. 1367-1371 ◽  
Author(s):  
Z E Wang ◽  
S L Reiner ◽  
S Zheng ◽  
D K Dalton ◽  
R M Locksley
Keyword(s):  
T Cells ◽  
Interferon Gamma ◽  
Knockout Mice ◽  
Leishmania Major ◽  
Interleukin 4 ◽  
Th2 Cells ◽  
Th1 Cells ◽  
Wild Type ◽  
Cd4 Cells ◽  
Ifn Gamma

Mice with homologous disruption of the interferon gamma (IFN-gamma) gene on the C57BL/6 background were infected with Leishmania major and the immune response assessed. In contrast to wild-type or heterozygous knockout mice, deficient animals were unable to restrict growth of the parasite and suffered lethal infection over 6-8 wk. Although wild-type and heterozygous littermates developed CD4+ cells that contained transcripts for IFN-gamma and lymphotoxin, typical of T helper type 1 (Th1) cells, the knockout mice developed CD4+ cells that contained transcripts for interleukin 4 (IL-4), IL-5, and IL-13, typical of Th2 cells. ELISPOT assays confirmed the reciprocal patterns of IFN-gamma or IL-4 production by T cells in similar frequencies in the respective groups of mice, and antibody analysis confirmed the presence of Th2-mediated isotype switching in the knockout mice. These data suggest that CD4+ T cells that normally respond to antigens by differentiation to Th1 cells default to the Th2 pathway in the absence of endogenous IFN-gamma.

scholarly journals Inhibition of murine erythroid colony formation in vitro by interferon gamma and correction by interferon receptor immunoadhesin

Blood ◽  
1994 ◽  
Vol 83 (4) ◽  
pp. 911-915 ◽  
Author(s):  
RT Jr Means ◽  
SB Krantz ◽  
J Luna ◽  
SA Marsters ◽  
A Ashkenazi
Keyword(s):  
Animal Model ◽  
Interferon Gamma ◽  
Colony Formation ◽  
Interleukin 1 ◽  
Inhibitory Effect ◽  
Dependent Manner ◽  
Ifn Gamma ◽  
Dose Dependent

It has been previously reported that inhibition of human erythroid colony-forming units (CFU-E) in vitro by interleukin-1 (IL-1) is an indirect effect, occurring through the production of interferon gamma (IFN gamma). IFN gamma, in turn, inhibits CFU-E colony formation directly, and its inhibitory effect can be overcome by exposure to high concentrations of erythropoietin (EPO). To develop an in vitro animal model for investigating inhibition of erythropoiesis by IFN gamma, the effects of recombinant murine (rm) IFN gamma on highly purified CFU-E from the spleens of mice infected with the anemia strain of the Friend virus (FVA) were studied. rmIFN gamma inhibited CFU-E colony formation in a dose-dependent manner. This inhibition occurred with large (> or = 8 cell) colonies only; smaller colonies were not affected. The inhibitory effect was corrected to 72% of control by high EPO concentrations of 64 U/mL. Murine CFU-E were then cultured with rmIFN gamma in the presence of a soluble murine IFN gamma receptor fused to the hinge and Fc domains of the human IgG1 heavy chain (mIFN gamma R-IgG). Inhibition of CFU-E colony formation by rmIFN gamma (100 U/mL) was corrected by mIFN gamma R-IgG in a dose-dependent manner, with an approximate IC50 of 0.05 nmol/L, and complete or near complete correction at 0.5 nmol/L. Similarly, a human IFN gamma R-IgG greatly reduced the inhibitory effect of recombinant human IFN gamma on human CFU-E. These experiments provide an in vitro animal model for studying the inhibitory effects of IFN gamma on erythropoiesis and indicate that IFN gamma R-IgG may be a useful agent for reducing the toxicity of IFN gamma in vivo.

Neuroinflammatory and behavioural changes in Atp7b knockout mice, an animal model for Morbus Wilson

2008 ◽  
Vol 35 (S 01) ◽  
Author(s):  
Y.N Löschmann ◽  
D Terwel ◽  
E Hoffmann ◽  
T Cantz ◽  
H Schöler ◽  
...  
Keyword(s):  
Animal Model ◽  
Knockout Mice ◽  
Morbus Wilson ◽  
Behavioural Changes

Transcriptome profile reveals AMPA receptor dysfunction in the hippocampus of the Rsk2-knockout mice, an animal model of Coffin–Lowry syndrome

2010 ◽  
Vol 129 (3) ◽  
pp. 255-269 ◽  
Author(s):  
Tahir Mehmood ◽  
Anne Schneider ◽  
Jérémie Sibillec ◽  
Patricia Marques Pereira ◽  
Solange Pannetier ◽  
...  
Keyword(s):  
Animal Model ◽  
Ampa Receptor ◽  
Knockout Mice ◽  
Transcriptome Profile
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