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180520s2012 xx |||||o 00| ||eng c |
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|a (DE-627)JST100198635
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|a (JST)23267317
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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|a Ouf, Eman Abou
|e verfasserin
|4 aut
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|a Ficolin-2 Levels and FCN2 Genetic Polymorphisms as a Susceptibility Factor in Schistosomiasis
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|c 2012
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|a Text
|b txt
|2 rdacontent
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|a Computermedien
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|2 rdamedia
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|a Online-Ressource
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|a Background. Human ficolin-2 (L-ficolins) encoded by the FCN2 gene are pattern-recognition proteins involved in innate immunity and are associated with several infectious diseases. Methods. A Nigerian cohort of 168 Schistosoma haematobium—infected individuals and 192 healthy controls were examined for functional single-nucleotide polymorphisms in the promoter region (-986G>A, -602G>A, -4A>G) and in exon 8 (+6424G>T) using real-time polymerase chain reaction. Results. The FCN2 -986A and -4G alleles were significantly associated with the occurrence of schistosomiasis (P = .0004 for -986G>A; P = .0001 for -4A>G). The heterozygous genotypes (P = .0006 for -986G>A; P = .0002 for -4A>G) were observed to be a risk factor for susceptibility to schistosomiasis, whereas the homozygous genotypes of major alleles (P = .0002 for -986G>A; P = .0001 for -4A>G) were observed to shield against schistosomiasis. The haplotype AGGG (P = .0002) was observed to be a risk factor for susceptibility to schistosomiasis compared with controls, and the haplotype GGAG (P = .04) was observed to confer protection compared with patients. Ficolin-2 serum level was significantly higher in controls (P < .005) and in controls with GGAG haplotypes (P < .0001). Conclusions. Our findings demonstrate that FCN2 promoter variants (-986G>A and -4A>G) influence ficolin-2 serum levels and susceptibility to schistosomiasis.
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|a Copyright © 2012 Oxford University Press on behalf of the Infectious Diseases Society of America
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|a Biological sciences
|x Biology
|x Genetics
|x Molecular genetics
|x Genes
|x Alleles
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|a Health sciences
|x Medical conditions
|x Diseases
|x Infectious diseases
|x Parasitic diseases
|x Helminthiasis
|x Trematode infections
|x Schistosomiasis
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|a Health sciences
|x Medical conditions
|x Infections
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4 |
|a Health sciences
|x Medical sciences
|x Medical research
|x Clinical research
|x Clinical trials
|x Control groups
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4 |
|a Biological sciences
|x Biology
|x Genetics
|x Genotypes
|x Haplotypes
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4 |
|a Biological sciences
|x Biology
|x Genetics
|x Genotypes
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4 |
|a Biological sciences
|x Biology
|x Anatomy
|x Excretory system
|x Excreta
|x Urine
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4 |
|a Biological sciences
|x Biology
|x Genetics
|x Medical genetics
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|a Biological sciences
|x Biology
|x Microbiology
|x Microorganisms
|x Pathogens
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4 |
|a Health sciences
|x Health care industry
|x Health care facilities
|x Hospitals
|x Hospital units
|x Hospital rooms
|x Operating rooms
|x MAJOR ARTICLES AND BRIEF REPORTS
|x PARASITES
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|a research-article
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|a Ojurongbe, Olusola
|e verfasserin
|4 aut
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|a Akindele, Akeem A.
|e verfasserin
|4 aut
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|a Sina-Agbaje, Olawumi R.
|e verfasserin
|4 aut
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|a Van Tong, Hoang
|e verfasserin
|4 aut
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|a Adeyeba, Adegboyega O.
|e verfasserin
|4 aut
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|a Kremsner, Peter G.
|e verfasserin
|4 aut
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|a Kun, Jürgen F. J.
|e verfasserin
|4 aut
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|a Velavan, TP
|e verfasserin
|4 aut
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|g volume:206
|g year:2012
|g number:4
|g pages:562-570
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|u http://dx.doi.org/10.1093/infdis/jis396
|3 Volltext
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|a GBV_USEFLAG_A
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|a GBV_JST
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|a AR
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|d 206
|j 2012
|e 4
|h 562-570
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