The 5' end of the NS-4 protein of different genotypes of hepatitis C virus (HCV) is highly variable in nucleotide and inferred amino acid sequence, with frequent predicted amino acid substitutions between all six of the major HCV genotypes described to date. This region has been shown to be antigenic by epitope mapping, and elicits antibody in HCV-infected individuals with a detectable type-specific component. We have used this sequence data to specify branched peptides for an indirect binding/competition assay to detect typespecific antibody to each major genotype. A total of 183 out of 210 samples (87%) from blood donors and patients with chronic hepatitis C infected with genotypes 1 to 6 showed detectable type-specific antibody to NS-4 peptides that in almost all cases (> 97 %) corresponded to the genotype detected by a PCR typing method. These findings demonstrate the existence of major antigenic differences between genotypes of HCV, and indicate how infection with different variants of HCV may be detected by a serological test.
Background: The role of the blood-brain barrier for cholesterol homeostasis in the brain is not known.Results: Significant influx of cholesterol into the brain and increased efflux of 24(S)-hydroxycholesterol were observed in mice with a defect blood-brain barrier.Conclusion: A defect blood-brain barrier increases permeability for steroid flux in both directions.Significance: Elucidation of the role of the blood-brain barrier for brain cholesterol turnover.
We previously described a heterozygous mouse model overexpressing human HA-tagged 24S-hydroxylase (CYP46A1) utilizing a ubiquitous expression vector. In this study, we generated homozygotes of these mice with circulating levels of 24OH 30–60% higher than the heterozygotes. Female homozygous CYP46A1 transgenic mice, aged 15 months, showed an improvement in spatial memory in the Morris water maze test as compared to the wild type mice. The levels of N-Methyl-D-Aspartate receptor 1, phosphorylated-N-Methyl-D-Aspartate receptor 2A, postsynaptic density 95, synapsin-1 and synapthophysin were significantly increased in the hippocampus of the CYP46A1 transgenic mice as compared to the controls. The levels of lanosterol in the brain of the CYP46A1 transgenic mice were significantly increased, consistent with a higher synthesis of cholesterol. Our results are discussed in relation to the hypothesis that the flux in the mevalonate pathway in the brain is of importance in cognitive functions.
BackgroundAnaemia during pregnancy can lead to adverse maternal and perinatal outcomes. The WHO recommends that all pregnant women in areas where anaemia is prevalent receive supplements of iron and folic acid. However, due to many factors, the use of iron and folic acid supplementation is still low in many countries. This study was conducted to assess the rates of iron-folic supplementation and the associated factors during pregnancy and the effects of taking iron-folic acid supplementation on rates of maternal anaemia and low birth weight (LBW) infants.MethodsA cross-sectional study was conducted at Khartoum Hospital, Sudan. Enrolled women answered a questionnaire on socio-demographics characteristics, their pregnancy and delivery.ResultsOf 856 women, 788 (92.1%) used iron-folic acid supplementation during pregnancy and 65.4% used folic acid. While place of residence, occupation and level of education were not associated with iron-folic acid usage, older age (OR = 3, CI = 1.4–6.3) and use of antenatal care (OR = 14.3, CI = 7.4–27.5) were associated with iron-folic acid use. Primiparity (OR = 3.8, CI = 1.9–7.6), maternal employment (OR = 3.9, CI = 2.25–6.77) and use of antenatal care (OR = 7.9, CI = 4.1–15) were the factors associated with folic acid. Using iron-folic acid was protective against anaemia (OR = 0.39, CI = 0.2–0.7) and LBW infants (OR = 0.3, CI = 0.17–0.68).ConclusionThere was a high rate of iron-folic acid supplementation use among pregnant women in Khartoum, Sudan, which was beneficial in preventing anaemia in expectant mothers and infants of LBW.
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