Effects of Wollastonite Fiber and Styrene-Butadiene Latex Polymer on the Long-Term Durability of Cement-Based Repair Materials.

Concrete structures are constructed in various geographical environments and climates, and frequently fail to fulfill their original functions over time due to issues such as aging and damage. Research on concrete structure repair materials is being conducted to solve these problems. This study evaluated the durability of a repair material composed of ultra-rapid hardening cement, styrene-butadiene (SB) latex polymer, and wollastonite mineral fiber. The performance targets were as follows: compressive strength of 20 MPa at 1 day of age and 45 MPa at 28 days of age, chloride ion charge passed of less than 1000 Coulombs, carbonation depth of 20 mm or less, and resistance to repeated freezing and thawing (relative dynamic modulus of elasticity) of 80% or more. The ultra-rapid hardening cement:silica sand ratio of 1:1.5 was the experimental variable, and the unit weight of each material in the mix proportion was determined to satisfy the flow requirement of 200 ± 5 mm. This flow ensured sufficient fluidity for spraying, which is the most widely used method for applying repair material. Wollastonite mineral fiber and SB latex polymer were added at 3% and 5% of the unit weight of the binder, respectively. The mechanical property of the repair material was evaluated through compressive strength, and durability was evaluated through chloride ion penetration, alkali resistance, resistance to carbonation, water absorption, and repeated freezing and thawing tests. The compressive strength satisfied both target values, regardless of the addition of SB latex polymer and wollastonite mineral fiber. The chloride ion penetration test, which was used as an indicator of durability, showed that mixtures without SB latex and wollastonite mineral fiber were not satisfied the target charge passed of 1000 Coulombs, while mixtures with latex and mineral fiber reached the target value. Notably, the co-addition of latex and wollastonite fiber showed the highest resistance to chloride ion penetration, alkali ion, carbonation, repeated freezing and thawing, and the least absorption. The results confirmed that the durability of the repair material based on ultra-rapid hardening cement was most effectively improved by the co-addition of SB latex polymer and wollastonite mineral fiber.

Bach2 represses the AP-1-driven induction of interleukin-2 gene transcription in CD4＋ T cells.

The transcription repressor Bach2 has been proposed as a regulator of T cell quiescence, but the underlying mechanism is not fully understood. Given the importance of interleukin-2 in T cell activation, we investigated whether Bach2 is a component of the network of factors that regulates interleukin-2 expression. In primary and transformed CD4＋ T cells, Bach2 overexpression counteracted T cell receptor/CD28- or PMA/ionomycin-driven induction of interleukin-2 expression, and silencing of Bach2 had the opposite effect. Luciferase and chromatin immunoprecipitation assays revealed that Bach2 binds to multiple Maf-recognition element-like sites on the interleukin-2 proximal promoter in a manner competitive with AP-1, and thereby represses AP-1-driven induction of interleukin-2 transcription. Thus, this study demonstrates that Bach2 is a direct repressor of the interleukin-2 gene in CD4＋ T cells during the immediate early phase of AP-driven activation, thereby playing an important role in the maintenance of immune quiescence in the steady state. [BMB Reports 2017; 50(9): 472-477].

Tissue transglutaminase is not involved in the aggregate formation of stably expressed alpha-synuclein in SH-SY5Y human neuroblastoma cells.

Intraneuronal deposition containing alpha-synuclein is implicated in the pathogenesis of synuclein-opathies including Parkinsons disease (PD). Although it has been demonstrated that cytoplasmic inclusions of wild type alpha-synuclein are observed in the brain of PD patients and that alpha-synuclein mutations such as A30P and A53T accelerate aggregate formation, the exact mechanism by which alpha-synuclein forms insoluble aggregates is still controversial. In the present study, to understand the possible involvement of tissue transglutaminase (tTG) in aggregate formation of alpha-synuclein, SH-SY5Y cell lines stably expressing wild type or mutant (A30P or A53T) alpha-synuclein were created and aggregate formation of alpha-synuclein was observed upon activation of tTG. The data demonstrated that alpha-synuclein negligibly interacted with tTG and that activation of tTG did not result in the aggregate formation of alpha-synuclein in SH-SY5Y cells overexpressing either wild type or mutant alpha-synuclein. In addition, alpha-synuclein was not modified by activated tTG in situ. These data suggest that tTG is unlikely to be a contributing factor to the formation of aggregates of alpha-synuclein in a stable cell model.