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| rdf:type
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| Description
| - Genetic analysis of resistance to infectious diseases revealed many important cues that led to new insights into the interaction between pathogen and host. This knowledge might help to better prognosis of disease and to development of novel therapeutics. I will concentrate on genes and loci that control susceptibility to diseases with an important epidemiologic impact such as AIDS, hepatitis B, tuberculosis, leprosy, schistosomiasis, and infection caused by parasite (malaria, leishmaniasis and trypanosomiasis). I will discuss also new perspectives of integration of human and mouse genetics that greatly contributes to our understanding of regulatory mechanisms in health and disease. I will discuss in more detail the questions of genetic analysis of susceptibility to disease caused of Trypanosoma spp. Protists Trypanosoma brucei gambiens cause human African trypanosomiasis, known as sleeping sickness. New world intracellular parasites T. (Schizotrypanum) cruzi cause Chagas’disease. Trypanosomas infect also laboratory mice and because the immune system in mice is very similar to human one, it can be assumed that the findings in mice have their analogy in humans. To analyze the multigenic control of response to Trypanosoma brucei brucei (T.b. brucei), we have used the recombinant congenic (RC) strains. The series of 20 CcS/Dem (CcS) RC strains is derived from two inbred strains, the background strain BALB/c and the donor strain STS/A (STS). Mice of RC strain CcS-11 survived shortest time after T. b. brucei infection and the strain was identified as a highly susceptible to the T. b. brucei infection. F2 hybrids between BALB/c and strain CcS-11 were used for subsequent genetic analysis. This analysis revealed four Tbbr ((T.b. brucei response) loci on chromosomes 3, 7, 12 and 19 affecting survival time after T. b. brucei infection. One of these loci on chromosome 12 is very short and contains only 26 genes. This will be the subject of our further research.
- Genetic analysis of resistance to infectious diseases revealed many important cues that led to new insights into the interaction between pathogen and host. This knowledge might help to better prognosis of disease and to development of novel therapeutics. I will concentrate on genes and loci that control susceptibility to diseases with an important epidemiologic impact such as AIDS, hepatitis B, tuberculosis, leprosy, schistosomiasis, and infection caused by parasite (malaria, leishmaniasis and trypanosomiasis). I will discuss also new perspectives of integration of human and mouse genetics that greatly contributes to our understanding of regulatory mechanisms in health and disease. I will discuss in more detail the questions of genetic analysis of susceptibility to disease caused of Trypanosoma spp. Protists Trypanosoma brucei gambiens cause human African trypanosomiasis, known as sleeping sickness. New world intracellular parasites T. (Schizotrypanum) cruzi cause Chagas’disease. Trypanosomas infect also laboratory mice and because the immune system in mice is very similar to human one, it can be assumed that the findings in mice have their analogy in humans. To analyze the multigenic control of response to Trypanosoma brucei brucei (T.b. brucei), we have used the recombinant congenic (RC) strains. The series of 20 CcS/Dem (CcS) RC strains is derived from two inbred strains, the background strain BALB/c and the donor strain STS/A (STS). Mice of RC strain CcS-11 survived shortest time after T. b. brucei infection and the strain was identified as a highly susceptible to the T. b. brucei infection. F2 hybrids between BALB/c and strain CcS-11 were used for subsequent genetic analysis. This analysis revealed four Tbbr ((T.b. brucei response) loci on chromosomes 3, 7, 12 and 19 affecting survival time after T. b. brucei infection. One of these loci on chromosome 12 is very short and contains only 26 genes. This will be the subject of our further research. (en)
- Genetic analysis of resistance to infectious diseases revealed many important cues that led to new insights into the interaction between pathogen and host. This knowledge might help to better prognosis of disease and to development of novel therapeutics. I will concentrate on genes and loci that control susceptibility to diseases with an important epidemiologic impact such as AIDS, hepatitis B, tuberculosis, leprosy, schistosomiasis, and infection caused by parasite (malaria, leishmaniasis and trypanosomiasis). I will discuss also new perspectives of integration of human and mouse genetics that greatly contributes to our understanding of regulatory mechanisms in health and disease. I will discuss in more detail the questions of genetic analysis of susceptibility to disease caused of Trypanosoma spp. Protists Trypanosoma brucei gambiens cause human African trypanosomiasis, known as sleeping sickness. New world intracellular parasites T. (Schizotrypanum) cruzi cause Chagas’disease. Trypanosomas infect also laboratory mice and because the immune system in mice is very similar to human one, it can be assumed that the findings in mice have their analogy in humans. To analyze the multigenic control of response to Trypanosoma brucei brucei (T.b. brucei), we have used the recombinant congenic (RC) strains. The series of 20 CcS/Dem (CcS) RC strains is derived from two inbred strains, the background strain BALB/c and the donor strain STS/A (STS). Mice of RC strain CcS-11 survived shortest time after T. b. brucei infection and the strain was identified as a highly susceptible to the T. b. brucei infection. F2 hybrids between BALB/c and strain CcS-11 were used for subsequent genetic analysis. This analysis revealed four Tbbr ((T.b. brucei response) loci on chromosomes 3, 7, 12 and 19 affecting survival time after T. b. brucei infection. One of these loci on chromosome 12 is very short and contains only 26 genes. This will be the subject of our further research. (cs)
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| Title
| - INFEKČNÍ NEMOCI Z POHLEDU GENETIKY
- INFEKČNÍ NEMOCI Z POHLEDU GENETIKY (cs)
- Infectious diseases – a genetic view (en)
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| skos:prefLabel
| - INFEKČNÍ NEMOCI Z POHLEDU GENETIKY
- INFEKČNÍ NEMOCI Z POHLEDU GENETIKY (cs)
- Infectious diseases – a genetic view (en)
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| skos:notation
| - RIV/68407700:21460/13:00213739!RIV14-MSM-21460___
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| http://linked.open...avai/predkladatel
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| http://linked.open...avai/riv/aktivita
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| http://linked.open...avai/riv/aktivity
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| http://linked.open...vai/riv/dodaniDat
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| http://linked.open...aciTvurceVysledku
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| http://linked.open.../riv/druhVysledku
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| http://linked.open...iv/duvernostUdaju
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| http://linked.open...titaPredkladatele
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| http://linked.open...dnocenehoVysledku
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| http://linked.open...ai/riv/idVysledku
| - RIV/68407700:21460/13:00213739
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| http://linked.open...riv/jazykVysledku
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| http://linked.open.../riv/klicovaSlova
| - infectious disease; susceptibility genes; controlling loci. (en)
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| http://linked.open.../riv/klicoveSlovo
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| http://linked.open...ontrolniKodProRIV
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| http://linked.open...v/mistoKonaniAkce
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| http://linked.open...i/riv/mistoVydani
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| http://linked.open...i/riv/nazevZdroje
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| http://linked.open...in/vavai/riv/obor
| |
| http://linked.open...ichTvurcuVysledku
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| http://linked.open...cetTvurcuVysledku
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| http://linked.open...vavai/riv/projekt
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| http://linked.open...UplatneniVysledku
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| http://linked.open...iv/tvurceVysledku
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| http://linked.open...vavai/riv/typAkce
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| http://linked.open.../riv/zahajeniAkce
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| number of pages
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| http://purl.org/ne...btex#hasPublisher
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| https://schema.org/isbn
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| http://localhost/t...ganizacniJednotka
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