18 research outputs found
Tough and flame-retardant poly(lactic acid) composites prepared via reactive blending with biobased ammonium phytate and in situ formed crosslinked polyurethane
The presence of phytase in yeasts isolated from the gastrointestinal tract of four major carps [Labeo rohita (Hamilton, 1822), Catla catla (Hamilton, 1822), Cirrhinus mrigala (Hamilton, 1822), Hypophthalmichthys molitrix (Valenciennes, 1844)], climbing pe
Evidence for epistasis between SLC6A4 and ITGB3 in autism etiology and in the determination of platelet serotonin levels
Abstract Autism is a neurodevelopmental disorder of unclear etiology. The consistent finding of platelet hyperserotonemia in a proportion of patients and its heritability within affected families suggest that genes involved in the serotonin system play a role in this disorder. The role in autism etiology of seven candidate genes in the serotonin metabolic and neurotransmission pathways and mapping to autism linkage regions (SLC6A4, HTR1A, HTR1D, HTR2A, HTR5A, TPH1 and ITGB3) was analyzed in a sample of 186 nuclear families. The impact of interactions among these genes in autism was assessed using the multifactor-dimensionality reduction (MDR) method in 186 patients and 181 controls. We further evaluated whether the effect of specific gene variants or gene interactions associated with autism etiology might be mediated by their influence on serotonin levels, using the quantitative transmission disequilibrium test (QTDT) and the restricted partition method (RPM), in a sample of 109 autistic children. We report a significant main effect of the HTR5A gene in autism (P = 0.0088), and a significant three-locus model comprising a synergistic interaction between the ITGB3 and SLC6A4 genes with an additive effect of HTR5A (P < 0.0010). In addition to the previously reported contribution of SLC6A4, we found significant associations of ITGB3 haplotypes with serotonin level distribution (P = 0.0163). The most significant models contributing to serotonin distribution were found for interactions between TPH1 rs4537731 and SLC6A4 haplotypes (P = 0.002) and between HTR1D rs6300 and SLC6A4 haplotypes (P = 0.013). In addition to the significant independent effects, evidence for interaction between SLC6A4 and ITGB3 markers was also found. The overall results implicate SLC6A4 and ITGB3 gene interactions in autism etiology and in serotonin level determination, providing evidence for a common underlying genetic mechanism and a molecular explanation for the association of platelet hyperserotonemia with autism
Timing and duration of anti–α4β1 integrin treatment after spinal cord injury: effect on therapeutic efficacy
A therapeutic time window for anti-CD11d monoclonal antibody treatment yielding reduced secondary tissue damage and enhanced behavioral recovery following severe spinal cord injury
Changes in chemical and anti-nutritional properties of pasta enriched with raw and germinated quinoa (Chenopodium quinoa Willd.) flours
The behaviour of myo-inositol hexakisphosphate in the presence of magnesium(II) and calcium(II): Protein-free soluble InsP6 is limited to 49 μM under cytosolic/nuclear conditions
Progress in the biology of myo-inositol hexakisphosphate (InsP6) has been delayed by the lack of a quantitative description of its multiple interactions with divalent cations. Our recent initial description of these [J. Torres, S. Dominguez, M.F. Cerda, G. Obal, A. Mederos, R.F. Irvine, A. Diaz, C. Kremer, J. Inorg. Biochem. 99 (2005) 828–840] predicted that under cytosolic/nuclear conditions, protein-free soluble InsP6 occurs as Mg5(H2L), a neutral complex that exists thanks to a significant, but undefined, window of solubility displayed by solid Mg5(H2L) · 22H2O (L is fully deprotonated InsP6). Here we complete the description of the InsP6–Mg2+–Ca2+ system, defining the solubilities of the Mg2+ and Ca2+ (Ca5(H2L) · 16H2O) solids in terms of Ks0 = [M2+]5[H2L10−], with pKs0 = 32.93 for M = Mg and pKs0 = 39.3 for M = Ca. The concentration of soluble Mg5(H2L) at 37 °C and I = 0.15 M NaClO4 is limited to 49 μM, yet InsP6 in mammalian cells may reach 100 μM. Any cytosolic/nuclear InsP6 in excess of 49 μM must be protein- or membrane-bound, or as solid Mg5(H2L) · 22H2O, and any extracellular InsP6 (e.g. in plasma) is surely protein-bound