Improvement of salt rejection efficiency of cellulose acetate membrane through modification by poly(amidoamine) dendrimer-functionalized graphene oxide.

In this work, the grafting method using graphene oxide (GO) - poly(amidoamine) dendrimer (PAMAM) nanocomposite as filler for the functionalization of cellulose acetate membrane is reported. Here, cellulose acetate membrane incorporated by nanocomposite in the polymer solution was prepared through the phase inversion technique. The effect of embedding GO-PAMAM on the characterization properties and rejection performance was studied. The results of zeta potential, thermogravimetric analysis (TGA), contact angle measurements, Fourier-transform infrared spectroscopy (FTIR), and field emission scanning electron microscopy (FE-SEM) established successful modification. Based on the data found, adding the filler improves membrane properties. Loading of 1.00 wt% of GO/PAMAM was found to be the optimized amount of the filler in the membrane processing with the highest porosity (74%), antifouling behavior (88%), reversible fouling ratio (45.71%), and the least contact angle (∼40°). Hence, the rejection and permeability tests of the prepared membrane were examined by Na2SO4 (98.40%), NaCl (52%), and MgCl2 (57%) solutions through a lab dead-end cell. According to the results, the value of salt rejection established more permeability and rejection than neat cellulose acetate membrane.

A lupus-susceptibility C57BL/6 locus on chromosome 3 (Sle18) contributes to autoantibody production in 129 mice.

Epistatic interactions between the non-autoimmune strains 129 and C57BL/6 (B6), used for generating gene-targeted animals, can induce a lupus-like disease. Genome-wide scan analyses of testcross progeny between these two strains have identified several lupus susceptibility loci, with the strongest linkage to the production of autoantibodies (auto-Abs) displayed by an interval on chromosome 1 of 129 origin (Sle16). However, the contribution of B6 loci to the lupus phenotype remained unknown. We used a congenic approach to deduce the contribution to the autoimmune traits of the B6 genomic interval on chromosome 3 (Sle18), previously shown to be linked to antinuclear Ab production. This interval, when transferred on a 129 background (a strain termed 129.B6-Sle18), promoted auto-Ab production targeting a broad spectrum of autoantigens, expansion of activated CD4(+)T and B cells and mild glomerulonephritis. Surprisingly, these immunological and serological defects were accompanied by a significant increase in the percentage of regulatory T cells (Tregs; CD4(+) Foxp3(+)). However, these cells, that expressed lower levels of Foxp3, had no impaired regulatory function when tested in vitro. These findings illustrate further the efficacy of congenic dissection for functional characterisation of individual lupus susceptibility loci and highlight the contribution of loci derived from non-autoimmune strains to the disease pathogenesis.

Identification of chromosome intervals from 129 and C57BL/6 mouse strains linked to the development of systemic lupus erythematosus.

Systemic lupus erythematosus is an autoimmune disease in which complex interactions between genes and environmental factors determine the disease phenotype. We have shown that genes from the non-autoimmune strains 129 and C57BL/6 (B6), commonly used for generating gene-targeted animals, can induce a lupus-like disease. Here, we conducted a genome-wide scan analysis of a cohort of (129 x B6)F2 C1q-deficient mice to identify loci outside the C1qa locus contributing to the autoimmune phenotype described in these mice. The results were then confirmed in a larger dataset obtained by combining the data from the C1q-deficient mice with data from previously reported wild-type mice. Both analyses showed that a 129-derived interval on distal chromosome 1 is strongly linked to autoantibody production. The B6 genome contributed to anti-nuclear autoantibody production with an interval on chromosome 3. Two regions were linked to glomerulonephritis: a 129 interval on proximal chromosome 7 and a B6 interval on chromosome 13. These findings demonstrate that interacting loci between 129 and B6 mice can cause the expression of an autoimmune phenotype in gene-targeted animals in the absence of any disrupted gene. They also indicate that some susceptibility genes can be inherited from the genome of non-autoimmune parental strains.