ABSTRACT
Plumage color can be considered as a social signal in chickens and a breeding identification tool among breeders. The relationship between plumage color and trait groups of immunity, growth and fertility is still a controversial issue. This research aimed to determine the genome-wide additive and epistatic variants affecting plumage color variation in chickens using the chicken Illumina 60k high-density SNP array. Two scenarios of genome-wide additive association studies using all SNPs and independent SNPs were carried out. To perform epistatic association analysis, the LD pruning approach was used to reduce the complexity of the analysis. We detected seven novel significant loci using all of the SNPs in the model and 14 SNPs using the LD pruning approach associated with plumage color. Moreover, 89 significantly associated SNP-SNP interactions (P-value <10-6 ) distributed in 25 chromosomes were identified, indicating that all of the signals together putatively influence the quantitative variation of plumage color. By annotating genes relevant to top SNPs, we have distinguished 18 potential candidate genes comprising HNF4beta, CKMT1B, TBC1D22A, RPL8, CACNA2D1, FZD4, SGMS1, IRF8, OPTN, LOC420362, TRABD, OvoDA1, DAD1, USP6, RBM12B, MIR1772, MIR1709 and MIR6696 and also 89 putative gene-gene combinations responsible for plumage color variation in chickens. Furthermore, several KEGG pathways including metabolic pathway, cytokine-cytokine receptor interaction, focal adhesion, melanogenesis, glycosaminoglycan biosynthesis-keratan sulfate and sphingolipid metabolism were enriched in the gene-set analysis. The results indicated that plumage color is a highly polygenic trait which, in turn, can be affected by multiple coding genes, regulatory genes and gene-gene epistasis interactions. In addition to genes with additive effects, epistatic genes with tiny individual effect sizes but significant effects in a pair have the potential to control plumage coloration in chickens.
Subject(s)
Avian Proteins/genetics , Chickens/physiology , Feathers/chemistry , Genome-Wide Association Study/veterinary , Pigmentation/genetics , Polymorphism, Single Nucleotide , Animals , Chickens/genetics , Female , MaleABSTRACT
OBJECTIVES: Human immunodeficiency virus (HIV) infection is a concerning problem in dentistry and HIV-infected patients may experience root caries due to different risk factors. The aim of this study was to find the prevalence of root caries in a selected Iranian HIV-positive population. METHODS: One hundred and seven IV drug users, based on ELISA and Western Blot test, were divided into two groups: group 1: HIV-positive patients and group 2: HIV-negative individuals. According to the T-CD4(+) cell count, subjects in group 1 were placed in two subgroups: Moderate immunodeficiency (200 mm(-3) < T-CD4(+) cells <500 mm(-3)) and Severe immunodeficiency patients (T-CD4(+) cells <200 mm(-3)). Teeth were examined by an examiner under suitable light to detect any changes in colour, texture or contour. The values of DMFT, DMFS, decayed root surfaces and total decayed surfaces were calculated. Data were analysed by independent t-test and chi-squared test. RESULTS: The mean DMFT, DMFS and decayed root caries in group 1 and 2 had no significant difference. The mean value of total decayed surfaces of HIV+ patients was significantly higher compared with HIV- individuals (P = 0.03). The comparison of all parameters between two subdivisions of group 1 showed no significant difference. CONCLUSIONS: The results indicate that HIV+ patients experienced more dental caries, but not more root caries than healthy ones. Along with decreasing T-CD4(+) cell count, tooth caries' prevalence did not increase. CLINICAL RELEVANCE: Based on our findings, root caries prevalence is almost the same in HIV-positive and negative individuals; however, it is necessary to decrease tooth caries by continual monitoring and periodic dental examination.
Subject(s)
HIV Seronegativity , HIV Seropositivity/complications , Root Caries/complications , Substance Abuse, Intravenous/complications , Adult , CD4 Lymphocyte Count , Chi-Square Distribution , DMF Index , Female , Humans , Iran , Male , Middle Aged , Morphine Dependence/complications , Retrospective Studies , Young AdultABSTRACT
It is shown experimentally that the electric charge of unsupported catalyst particles has a major influence on the methanation of CO with nano-sized Ni particles as catalyst at temperatures between 680 K and 720 K. Neutral particles showed an apparent activation energy of 148 kJ/mol, significantly higher than the apparent activation energies of 43 kJ/mol and 60 kJ/mol for negatively and positively charged particles, respectively. The obtained activation energies are comparable to energies obtained for different sites on alumina supported nickel catalysts. The change in activation energy can be qualitatively explained by different electron interchange between the chemisorbed species and the catalyst. We suggest that the observed effect of electron enhancement or depletion on catalysis is also a governing effect in strong metal support interaction (SMSI), where the displacement of electrons is related to the contact potential between catalyst and substrate.
ABSTRACT
BACKGROUND AND AIM OF THE STUDY: The recent clinical history and experimental studies of the Medtronic Parallel (MP) valve suggest that bileaflet valve leakage flow is a primary initiator of thrombosis. These studies investigated the effects of physiologic leakage flow through a MP valve on various markers of blood damage. METHODS: A centrifugal pump was used to drive whole, human blood anticoagulated with PPACK through a circuit containing a MP 27 mm valve in the closed position (experimental runs) or a MP 27 mm valve in the open position (control runs). Samples were taken at set time intervals after the start of the pump. These samples were analyzed by cell counting, flow cytometry, and ELISA. RESULTS: Cell counts remained relatively constant in both the experimental and control runs. Increases in plasma hemoglobin concentration and the percentage of glycophorin A-positive fragments in the cell population were not significant in either the experimental or the control runs. Plasma platelet factor 4 activity and the percentage of the CD41-positive population which was positive for annexin V increased significantly (p <0.05) in the experimental runs compared with the control runs. CONCLUSION: The results indicate that bileaflet valve leakage flow causes significant platelet disruption, that erythrocytes are more resistant to disruption by leakage flow than platelets and granulocytes, and that annexin V binding to platelets and plasma platelet factor 4 activity are more sensitive markers of leakage induced blood damage than plasma hemoglobin concentration.