Characterization and flocculation performance of a newly green flocculant derived from natural bagasse cellulose.

A newly green natural polymer bagasse cellulose based flocculant (PBCF) was synthesized utilizing a grafting copolymerization method for effectively enhancing humic acid (HA) removal from natural water. This work aims to investigate flocculation behavior of PBCF in synthetic water containing HA, and the effects of flocculant dose and initial solution pH on flocculation performance. Results showed that PBCF functioned well at a flocculant dose of 60 mg/L and pH ranging from 6.0 to 9.0. The organic removal efficiency in synthetic water in terms of HA (UV254) and chemical oxygen demand (COD Mn) were up to 90.6% and 91.3%, respectively. Furthermore, the charge neutralization and adsorption bridging played important roles in HA removal. When applied for lake water, PBCF removed 91.6% turbidity and 50.0% dissolved organic matter, respectively. In short, PBCF demonstrates great potential in water treatment in a safe and environmentally friendly or 'green' way.

Role of SIRT2 in regulating the dexamethasone-activated autophagy pathway in skeletal muscle atrophy.

The proteolytic autophagy system is involved in a major regulatory pathway in dexamethasone (Dex)-induced muscle atrophy. Sirtuin 2 (SIRT2) is known to modulate autophagy signaling, exerting effects in skeletal muscle atrophy. We examined the effects of SIRT2 on autophagy in Dex-induced myoatrophy. Tostudy this, mice were randomly distributed among the normal, Dex, and sirtinol groups. C2C12 cells were differentiated into myotubes and transduced with lentivirus carrying Sirt2-green fluorescent protein (GFP) or Sirt2 short hairpin RNA (Sirt2-shRNA)-GFP. To evaluate the mass and function of skeletal muscles, we measured myofiber cross-sectional area, myotube size, gastrocnemius (GA) muscle wet mass:body mass ratio (%), and time to exhaustion. The expression levels of SIRT2, myosin heavy chain, microtubule-associated protein 1 light chain 3 (LC3), and Beclin-1 were measured using Western blotting and quantitative reverse transcription - polymerase chain reaction. Inhibition of SIRT2 markedly attenuated GA muscle mass and endurance capacity. The same phenotype was observed in Sirt2-shRNA-treated myotubes, as evidenced by their decreased size. Conversely, overexpression of SIRT2 alleviated Dex-induced myoatrophy in vitro. Moreover, SIRT2 negatively regulated the expression of LC3b and Beclin-1 in skeletal muscles. These findings suggest that SIRT2 activation protects myotubes against Dex-induced atrophy through inhibition of the autophagy system; this phenomenon may serve as a target for treating glucocorticoid-induced myopathy.