Analysis Tools
mortality/aging
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• all mice infected with Plasmodium chabaudi chabaudi die unlike control mice without an increase in parasitemia
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• only ~20% of newborn homozygotes are obtained from heterozygote breedings, suggesting partial perinatal lethality
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• at 3 weeks, only about 7% of homozygotes are obtained from heterozygote matings; surviving homozygotes appear grossly normal
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cardiovascular system
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• in response to chronic hypoxia (10% oxygen, 7 weeks), homozygotes display mononuclear inflammatory cell infiltration and extensive cardiomyocyte degeneration and death with focal calcification, characteristic of infarcts which are 1-2 weeks old
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• in response to chronic hypoxia (10% oxygen, 7 weeks), homozygotes exhibit a greater increase in right ventricular weight relative to wild-type mice
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• in response to chronic hypoxia (10% oxygen, 5-7 weeks), homozygotes show comparable increases in hematocrit values, pulmonary hypertension (right ventricular systolic pressure) and pulmonary vascular remodeling (peripheral muscularized vessels) relative to wild-type mice
• however, in response to chronic hypoxia (10% oxygen, 5 weeks), homozygotes exhibit increased right ventricular dilation relative to wild-type mice, with severe dilation noted at 7 weeks
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• in response to chronic hypoxia (10% oxygen, 7 weeks), homozygotes exhibit increased perivascular fibrosis, with earlier collagen deposition and scar formation surrounding infarcted sites relative to wild-type mice
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• in response to chronic hypoxia (10% oxygen, 7 weeks), 4 of 6 homozygotes exhibit evidence of right ventricular infarcts which are less than 2 weeks old
• however, no left ventricular infarcts or coronary occlusion are observed
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homeostasis/metabolism
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• in response to chronic hypoxia (10% oxygen, 7 weeks), 4 of 6 homozygotes exhibit evidence of right ventricular infarcts which are less than 2 weeks old
• however, no left ventricular infarcts or coronary occlusion are observed
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• 4-fold in mice infected with Plasmodium chabaudi chabaudi
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• in response to chronic hypoxia (10% oxygen, 7 weeks), all (4 of 4) homozygotes with right ventricular infarcts display large, organized mural thrombi
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• in mice infected with Plasmidium berhei ANKA
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cellular
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• in response to chronic hypoxia (10% oxygen, 7 weeks), homozygotes display increased cardiomyocyte apoptosis, as shown by increased TUNEL-positive cells in infarcted areas
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• in response to chronic hypoxia (10% oxygen, 7 weeks), homozygotes show extensive lipid peroxidation and oxidative damage in the zone of right ventricular infarctions
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muscle
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• in response to chronic hypoxia (10% oxygen, 7 weeks), homozygotes display mononuclear inflammatory cell infiltration and extensive cardiomyocyte degeneration and death with focal calcification, characteristic of infarcts which are 1-2 weeks old
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• in response to chronic hypoxia (10% oxygen, 7 weeks), homozygotes display increased cardiomyocyte apoptosis, as shown by increased TUNEL-positive cells in infarcted areas
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immune system
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• mice infected with Plasmodium chabaudi chabaudi (PCC) exhibit increased mortality and hepatic failure with a 4-fold increase in alanine aminotransferase plasma concentration and accumulation of thiobarbituric acid reactive substances compared with control mice
• mice infected with Plasmidium berhei ANKA exhibit increased cerebral malaria as indicated by brain edema compared with control mice
• however, mice infected with PCC exhibit normal parasitemia and do not develop cerebral malaria or kidney failure
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• all mice infected with Plasmodium chabaudi chabaudi die unlike control mice without an increase in parasitemia
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liver/biliary system
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• in mice infected with Plasmodium chabaudi chabaudi
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nervous system
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• in mice infected with Plasmidium berhei ANKA
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| malaria | DOID:12365 | J:153083 | ||
