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Introduction Controversy exists around the immunogenicity of the various formulations of botulinum neurotoxin type A (BoNT-A). Methods A systematic review of the literature (1968–2013) was performed, including review of materials from the FDA. Neutralizing antibody rates were calculated for overall BoNT-A and for each commercially available BoNT-A (abobotulinumtoxinA, incobotulinumtoxinA, onabotulinumtoxinA), and were compared by using the Chi-squared test. Two different onabotulinumtoxinA products were identified during the specified time-frame and classed as ‘old’ and ‘new’ versions. Results A total of 31 studies involving 5811 subjects met inclusion criteria and were analyzed. Therapeutic indications included: cervical dystonia, blepharospasm, spasticity, glabellar lines, hyperactive detrusor/sphincter dysfunction. The overall rate of development for neutralizing antibodies to BoNT-A was 2.1%. Individual rates were 1.4% for abobotulinumtoxinA, 0.8 to 1.1% for incobotulinumtoxinA, 7.2% for old onabotulinumtoxinA and 3.6% for new onabotulinumtoxinA. No significant differences were found between abobotulinumtoxinA and incobotulinumtoxinA rates (OR 1.82 [95%CI] [0.96–3.43], p = 0.066; OR 1.30 [0.69–2.46], p = 0.415). Rates of neutralizing antibodies were significantly lower with abobotulinumtoxinA and incobotulinumtoxinA versus either onabotulinumtoxinA formulations. Conclusions The overall neutralizing antibody rate for BoNT-A was low (≤2.1%). The rate of developing neutralizing antibodies was similar between abobotulinumtoxinA and incobotulinumtoxinA, both significantly lower when compared with onabotulinumtoxinA. [ABSTRACT FROM AUTHOR]

Intravenous immunoglobulin (IVIg) is increasingly being used in the treatment of a wide range of autoimmune and systemic inflammatory diseases involving distinct pathogenesis. However, the mechanism by which IVIg exerts its sustained therapeutic effects in these diverse diseases has remained enigmatic. Recent findings from experimental and clinical research have, however, provided new insights into the mechanisms of action of IVIg. IVIg targets various cellular (such as dendritic cells, macrophages, monocytes, B and T cells) and soluble compartments (cytokines, complements, autoantibodies and autoantigens) of the immune system that are involved in the pathogenesis of autoimmune diseases. Thus, the mechanisms of actions of IVIg are mutually non-exclusive and work in synergy to contribute to its therapeutic effects. [Copyright &y& Elsevier]

Carboxylic acid mono functional poly(methyl methacrylate) was prepared by emulsion photopolymerization using 4-diethylthiocarbamoylsulfanylmethyl benzoic acid (DTBA) as sur-iniferter agent. DTBA is efficient to obtain mono functional polymers with a linear evolution of Mn vs. monomer conversion up to 60%. Beyond 60% monomer conversion, Mn decreases drastically and addition of a supplementary surfactant seems to disturb the effect of sur-iniferter. Secondly, an α-functional polymer presenting a Mn=43500 g/mol, a polydispersity index Ip=2.67 and a functionality fCOOH=98% was grafted in the molten state onto a statistical copolymer of ethylene and glycidyl methacrylate and the amount of PMMA grafts was about 10 wt%. In a final step, the graft copolymer was used as emulsifier in LDPE/PVDF blends. Blends including the graft copolymer present a better interfacial adhesion and a reduction of the size of the dispersed phase in comparison with blends without additive. [Copyright &y& Elsevier]

• CO 2 -soluble Pd-complexing polymers bearing pyridine units have been synthesized. • Cloud point curves of the polymers have been determined in dense CO 2. • Extraction of Pd from supported catalysts was performed in CO 2 at 40 °C and 25 MPa. • Strong effect of the Pd oxidation state on extraction in CO 2 was reported. • 73 % of Pd was extracted from the catalytic support by the complexing polymers. Precious metals, in particular palladium (Pd), have a wide range of daily applications, from automotive catalysts to fine chemistry production. Nevertheless, these metals are relatively rare and highly expensive, considering their massive industrial utilization. In the last decades, different recycling methods have been explored. Nowadays, the most applied methods, namely pyro- and/or hydrometallurgy, involve energy-intensive processes and/or the generation of large amounts of effluents to be treated. Thus, the development of a more sustainable recycling process of precious metals is highly desirable. In the present work, we introduce a sustainable process based on the use of a green solvent, supercritical CO 2 , operated under mild conditions (P = 25 MPa and T = 40 °C). The extraction process is possible thanks to the addition of CO 2 -soluble complexing polymers bearing pyridine units. The proposed method leads to the extraction of more than 70 % of Pd from an aluminosilica-supported catalyst. [ABSTRACT FROM AUTHOR]

Background T H 17 cells play a critical role in the pathogenesis of several autoimmune and allergic diseases. Intravenous immunoglobulin (IVIg), a therapeutic preparation of polyclonal IgG that is increasingly used in the treatment of diverse autoimmune and allergic diseases, might target T H 17 cells to exert therapeutic effects. Objective We sought to examine whether IVIg interferes with the development and function of human T H 17 cells. Methods T H 17 cells were differentiated from naive human CD4 + T cells in the presence of TGF-β and IL-21. T H 17 cells were amplified by stimulating memory CD4 + T cells in the presence of IL-1β and IL-6. The effect of IVIg was examined on the differentiation and amplification of T H 17 cells, expression of the T H 17 lineage-specific transcription factor retinoic acid-related orphan receptor C, secretion of T H 17 effector cytokines, and phosphorylation of signal transducer and activator of transcription 3, a transcription factor that plays an important role in T H 17 cell development and function. Results IVIg inhibits the differentiation and amplification of human T H 17 cells, as well as the production of their effector cytokines IL-17A, IL-17F, IL-21, and CCL20. The inhibitory effects of IVIg on T H 17 cells are F(ab′) 2 dependent and involve interference with the expression of retinoic acid-related orphan receptor C and activation of signal transducer and activator of transcription 3. Also, IVIg significantly enhanced forkhead box protein 3–positive regulatory T cells among the memory CD4 + T cells. Conclusion These results reveal a novel mechanism of action of IVIg in achieving a therapeutic effect in autoimmune and allergic diseases, in which T H 17 cells play a key modulatory role in sustaining the chronic inflammatory response. Our results also suggest a reciprocal regulation of T H 17 and regulatory T-cell populations by IVIg. [ABSTRACT FROM AUTHOR]