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dc.contributor.authorAsgharzadeh, M
dc.contributor.authorMazloumi, A
dc.contributor.authorKafil, HS
dc.contributor.authorGhazanchaei, A
dc.date.accessioned2018-08-26T06:33:43Z
dc.date.available2018-08-26T06:33:43Z
dc.date.issued2007
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/43814
dc.description.abstractVisceral leishmaniasis is an infectious disease caused by various species of Leishmania and Leishmania infantum is known to be associated with VL in Iran. Different factors can consider risk factors for VL that some remain unknown. The aim of present study is to determine the distribution of the alleles ofmannose-binding lectin gene codon 52, 54, 57 and promoter variants H/L, X/Y, P and Q in confirmed VL patients while compares then with normal controls and seek correlation between these variants and confirmed VL patients. Fifty eight confirmed VL patients blood samples were compared with one hundred and twenty normal controls from Azarbaijan population of Iran. MBL genotypes were investigated by polymerase chain reaction and restriction fragment length polymorphism. Allelic and genotypic frequency of the polymorphism at promoters and genes didn't show statistical differences in patients and normal controls, but frequency of alleles with high MBL concentration in VL patients was higher than controls (p = 0.03). We can conclude that normal alleles with high MBL serum level are risk factor for VL and defective alleles have protective role in VL.
dc.language.isoEnglish
dc.relation.ispartofPakistan journal of biological sciences : PJBS
dc.subjectAnimals
dc.subjectBase Sequence
dc.subjectDNA Primers
dc.subjectHumans
dc.subjectLeishmania infantum
dc.subjectLeishmaniasis, Visceral
dc.subjectMannose-Binding Lectin
dc.subjectPolymerase Chain Reaction
dc.subjectPolymorphism, Genetic
dc.subjectPolymorphism, Restriction Fragment Length
dc.subjectPromoter Regions, Genetic
dc.titleMannose-binding lectin gene and promoter polymorphism in visceral leishmaniasis caused by Leishmania infantum.
dc.typearticle
dc.citation.volume10
dc.citation.issue11
dc.citation.spage1850
dc.citation.epage4
dc.citation.indexPubmed


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