Ganglioside composition of a mouse brain tumor grown in the severe combined immunodeficiency (SCID) mouse

1998 ◽  
Vol 33 (1) ◽  
pp. 27-37 ◽  
Author(s):  
Thomas N. Seyfried ◽  
Mohga El-Abbadi ◽  
Jeffrey A. Ecsedy ◽  
Mary E. Griffin ◽  
Herbert C. Yohe
Keyword(s):  
Brain Tumor ◽  
Mouse Brain ◽  
Scid Mouse ◽  
Severe Combined Immunodeficiency ◽  
Combined Immunodeficiency ◽  
Ganglioside Composition

scholarly journals In vivo sequestration of Plasmodium falciparum-infected human erythrocytes: a severe combined immunodeficiency mouse model for cerebral malaria.

1995 ◽  
Vol 182 (3) ◽  
pp. 643-653 ◽  
Author(s):  
K Willimann ◽  
H Matile ◽  
N A Weiss ◽  
B A Imhof
Keyword(s):  
Plasmodium Falciparum ◽  
Mouse Model ◽  
Cerebral Malaria ◽  
Mouse Brain ◽  
Scid Mouse ◽  
Severe Combined Immunodeficiency ◽  
Human Erythrocytes ◽  
Combined Immunodeficiency ◽  
The Brain

Cerebral malaria is a fatal complication of infection by Plasmodium falciparum in man. The neurological symptoms that characterize this form of malarial disease are accompanied by the adhesion of infected erythrocytes to the vasculature of the brain. To study this phenomenon in vivo, an acute phase severe combined immunodeficiency (SCID) mouse model was developed in which sequestration of P. falciparum-infected human erythrocytes took place. During acute cerebral malaria in humans, the expression of intercellular adhesion molecule-1 (ICAM-1) is induced in vascular endothelium by inflammatory reactions. Acute phase ICAM-1 expression can also be obtained in SCID mice. The endothelium of the midbrain region was the most responsive to such inflammatory stimulus. It is noteworthy that the reticular formation in the midbrain controls the level of consciousness, and loss of consciousness is a symptom of cerebral malaria. We found that infected human erythrocytes were retained 24 times more than normal erythrocytes in ICAM-1-positive mouse brain. Sequestration to the brain was reduced by anti-ICAM-1 antibodies. These in vivo results were confirmed by the binding of P. falciparum-infected erythrocytes to the ICAM-1-positive endothelium in tissue sections of mouse brain. We conclude that the SCID mouse serves as a versatile in vivo model that allows the study of P. falciparum-infected erythrocyte adhesion as it occurs in human cerebral malaria. Upregulation of ICAM-1 expression in the region of the midbrain correlates with increased retention of malaria-infected erythrocytes and with the symptoms of cerebral malaria.

scholarly journals The therapeutic use of osmotic minipumps in the severe combined immunodeficiency (SCID) mouse model for rheumatoid arthritis

2008 ◽  
Vol 68 (1) ◽  
pp. 124-129 ◽  
Author(s):  
A Knedla ◽  
B Riepl ◽  
S Lefèvre ◽  
S Kistella ◽  
J Grifka ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Mouse Model ◽  
Scid Mouse ◽  
Severe Combined Immunodeficiency ◽  
Protective Effects ◽  
Combined Immunodeficiency ◽  
Human Cartilage ◽  
Osmotic Minipumps ◽  
Osmotic Pumps ◽  
Scid Mouse Model

Objectives:The viral gene transfer of interleukin 1 receptor antagonist (IL1ra) and interleukin 10 (IL10) into rheumatoid arthritis (RA) synovial fibroblasts (RASFs) has shown protective effects on cartilage destruction in the severe combined immunodeficiency (SCID) mouse model of RA. Nevertheless, side effects of viral transduction are possible and a number of cytokines or cytokine inhibitors are not available encoded in viral vehicles. As the production of viruses coding for bioactive proteins is cost and time intensive, we established an in vivo long-term release model using osmotic minipumps in the SCID mouse model for RA.Methods:Isolated RASFs were cultured for four passages and coimplanted together with human cartilage and an Alzet osmotic miniature pump model 2004, containing 200 μl of IL10 and IL1ra for 40 days in SCID mice. Implants were removed after 40 days and evaluated histologically. The actual rates of IL10 and IL1ra in murine serum were measured by ELISA.Results:Release of IL10 and IL1ra by the pumps was effective as both could be measured in significant amounts in the serum of the mice. IL10 and IL1ra release showed protective effects towards the coimplanted cartilage, similar to the adenovirally IL10/IL1ra-transduced RASFs. The mean (SD) invasion scores for the implants with the osmotic pumps were: invasion 0.7 (0.5), degradation 0.5 (0.3) (all parameters significant vs controls, p<0.05).Conclusions:The results demonstrate that the combination of osmotic pumps with the SCID mouse model for RA can be used as approach for application and evaluation of cartilage-protective molecules. Furthermore, the effect of cartilage-protective cytokines is independent of the type of application.

scholarly journals Childhood acute myeloid leukemia in mice with severe combined immunodeficiency

Blood ◽  
1994 ◽  
Vol 84 (1) ◽  
pp. 20-26
Author(s):  
LM Chelstrom ◽  
R Gunther ◽  
J Simon ◽  
SC Raimondi ◽  
R Krance ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Scid Mouse ◽  
Severe Combined Immunodeficiency ◽  
Scid Mice ◽  
Leukemic Cells ◽  
Human Leukemia ◽  
Combined Immunodeficiency ◽  
Kidney Capsule ◽  
Acute Myeloid

Primary bone marrow blasts from 4 children with t(8;21) acute myeloid leukemia (AML), 6 children with inv(16) AML, and 2 children with t(9;11) AML were injected intravenously or transplanted under the kidney capsule of sublethally irradiated mice with severe combined immunodeficiency (SCID). Leukemic cells from all AML patients infiltrated the SCID mouse thymus, suggesting that the thymic microenvironment supports the survival and growth of human AML blasts. Blasts from 1 of 4 t(8;21) AML patients and 4 of 6 inv(16) AML patients caused histopathologically detectable disseminated leukemia. Blasts from the remaining patients produced disseminated occult leukemia that was only detected by polymerase chain reaction. Occurrence of histopathologically detectable disseminated leukemia was dependent on intravenous injection of leukemic cells; none of the mice challenged with an inoculum transplanted under the kidney capsule developed overt leukemia. No obvious association was noted between occurrence of leukemia in SCID mice and clinical or laboratory features presented by patients, including age, sex, or leukocyte count at diagnosis. To our knowledge, this study is the first to show that leukemic blasts from children with newly diagnosed AML, especially inv(16) AML, can cause disseminated human leukemia in SCID mice without exogenous cytokine support. The SCID mouse model system may prove particularly useful for designing more effective treatment strategies against childhood AML.

scholarly journals Childhood acute myeloid leukemia in mice with severe combined immunodeficiency

Blood ◽  
1994 ◽  
Vol 84 (1) ◽  
pp. 20-26 ◽  
Author(s):  
LM Chelstrom ◽  
R Gunther ◽  
J Simon ◽  
SC Raimondi ◽  
R Krance ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Scid Mouse ◽  
Severe Combined Immunodeficiency ◽  
Scid Mice ◽  
Leukemic Cells ◽  
Human Leukemia ◽  
Combined Immunodeficiency ◽  
Kidney Capsule ◽  
Acute Myeloid

Abstract Primary bone marrow blasts from 4 children with t(8;21) acute myeloid leukemia (AML), 6 children with inv(16) AML, and 2 children with t(9;11) AML were injected intravenously or transplanted under the kidney capsule of sublethally irradiated mice with severe combined immunodeficiency (SCID). Leukemic cells from all AML patients infiltrated the SCID mouse thymus, suggesting that the thymic microenvironment supports the survival and growth of human AML blasts. Blasts from 1 of 4 t(8;21) AML patients and 4 of 6 inv(16) AML patients caused histopathologically detectable disseminated leukemia. Blasts from the remaining patients produced disseminated occult leukemia that was only detected by polymerase chain reaction. Occurrence of histopathologically detectable disseminated leukemia was dependent on intravenous injection of leukemic cells; none of the mice challenged with an inoculum transplanted under the kidney capsule developed overt leukemia. No obvious association was noted between occurrence of leukemia in SCID mice and clinical or laboratory features presented by patients, including age, sex, or leukocyte count at diagnosis. To our knowledge, this study is the first to show that leukemic blasts from children with newly diagnosed AML, especially inv(16) AML, can cause disseminated human leukemia in SCID mice without exogenous cytokine support. The SCID mouse model system may prove particularly useful for designing more effective treatment strategies against childhood AML.

Propagation of Human Papillomavirus Type 11 in Human Xenografts Using the Severe Combined Immunodeficiency (SCID) Mouse and Comparison to the Nude Mouse Model

Virology ◽  
1993 ◽  
Vol 197 (1) ◽  
pp. 455-458 ◽  
Author(s):  
William Bonnez ◽  
Robert C. Rose ◽  
Carrie Da Rin ◽  
Christine Borkhuis ◽  
Karen L. de Mesy Jensen ◽  
...  
Keyword(s):  
Human Papillomavirus ◽  
Mouse Model ◽  
Nude Mouse ◽  
Scid Mouse ◽  
Severe Combined Immunodeficiency ◽  
Combined Immunodeficiency ◽  
Nude Mouse Model
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