Discharge from sewage treatment plants (STPs) is a significant pathway of entry for microplastics (MPs) to the environment. Therefore, STPs should be considered as an important barrier to the distribution and circulation of MPs in the aquatic environment. In this study, the fate and material-specific properties of MPs were investigated in an STP-equipped and granule-activated carbon (GAC) tower with a thermal regeneration system. This system functioned with a tertiary treatment unit. The GAC with thermal regeneration removed 92.8% of MPs and was useful for removing MPs with a specific gravity less than that of water and with a size of 20–50 µm, which had negligible removal in the conventional STP process. In addition, a lab-scale electric-coagulation experiment was conducted to examine its potential utility as a pretreatment process for further enhancing the removal efficiency of MPs by GAC. After 30 min of electro-coagulation using aluminum electrodes, 90% of MPs were converted into separable flocs by centrifugation. These flocs may be effectively removed by GAC or other tertiary treatment steps. This study demonstrates that GAC with thermal regeneration is a tertiary process that can efficiently prohibit the release of MPs from STPs and circulation of MPs in the natural environment.

To investigate the CGE on hair growth and to explore the mechanism that is involved in the acceleration of anagen induction, we investigated the effects of CGE studied on cell proliferation and molecular mechanism in human hair dermal papilla cells (hDPCs) and keratinocytes (HaCaT cells). Additionally, hair growth evaluation was carried out following topical treatment of the dorsal skin of telogen C57BL/6 mice with CGE for 14 days. As result, CGE increased cell viability and ALP activity in hDPCs. Moreover, CGE increased the expression of catenin beta 1 (CTNNB1), ALP, sex-determining region Y-box 2 (SOX2), insulin-like growth factor 1 (IGF1), and vascular endothelial growth factor A (VEGFA) genes in hDPCs. CGE increased the expression of proteins such as ALP, β-catenin, and phosphorylation of glycogen synthase kinase 3β (pGSK3β), and protein kinase B (pAKT) in hDPCs. Furthermore, CGE induced the proliferation of HaCaT cells and up-regulated AKT-ERK-GSKβ-β-catenin signaling in HaCaT cells. Additionally, the anagen induction effects of CGE were confirmed on the telogen-anagen transition mice model. these findings demonstrated that CGE promoted the entering the growth phase of hair follicle via activation of β-catenin signaling pathways in vivo. Thus, this study suggests that CGE might be a potential therapeutic reagent for hair growth.

A cream-coloured, Gram-stain-negative, rod-shaped bacterium, designated strain KSC-6T, was isolated from soil sampled at the Gapcheon River watershed in Daejeon, Republic of Korea. The organism does not require NaCl for growth and grows at pH 6.0–8.0 (optimum, pH 7.0) and 10–37 °C (optimum, 25 °C). Phylogenetic trees based on the 16S rRNA gene sequences reveal that strain KSC-6T belongs to the family Chitinophagaceae within the order Chitinophagales and is most closely related to Panacibacter ginsenosidivorans Gsoil 1550T (95.9% similarity). The genomic DNA G+C content was 38.9 mol%. The major cellular fatty acids (>8 %) of strain KCS-6T were iso-C15:0, iso-C15 : 1 G and iso-C17 : 0 3-OH. The predominant respiratory quinone was menaquinone 7 and the predominant polar lipids were phosphatidylethanolamine, five unidentified aminolipids and two unidentified lipids. Based on genome analyses, low digital DNA–DNA hybridization, average nucleotide identity and average amino acid identity values with closely related genera, and differential chemotaxonomic and physiological properties, we suggest that strain KCS-6T represents a novel species in a new genus in the family Chitinophagaceae , for which the name Limnovirga soli gen. nov., sp. nov. (type strain KCS-6T=KCCM 43337T=NBRC 114336T) is proposed.

The huge diversity of secondary bioactive metabolites, such as antibiotic and anticancer compounds produced by Micromonospora sp., makes it an attractive target for study. Here, we explored the anti-proliferative activities of Micromonospora sp. M2 extract (MBE) in relation to its pro-oxidative activities in A549 and MCF7 cell lines. Anti-proliferative effects were assessed by treating cells with MBE. We found that treatment with MBE decreased cell proliferation and increased intracellular reactive oxygen species, and that these observations were facilitated by the suppression of the PI3K-AKT pathway, alterations to the Bcl/Bad ratio, and increased caspase activity. These observations also demonstrated that MBE induced apoptotic cell death in cell lines. In addition, the phosphorylation of P38 and JNK were upregulated following MBE treatment in both cell lines. Collectively, these results indicate that MBE acts as an anticancer agent via oxidative stress and JNK/MAPK pathway activation, enhancing apoptotic cell death in cell lines.

In the present study, we investigated the mechanisms underlying the anti-inflammatory effects of rosmarinosin A in (LPS)-stimulated RAW 264.7 macrophages. The cells were pretreated with various concentrations of rosmarinosin A, and then stimulated with LPS. Rosmarinosin A reduced the production of nitric oxide (NO) and prostaglandin E₂ (PGE₂), possibly through the modulation of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression, respectively. Additionally, it inhibited the production of pro-inflammatory cytokines, such as tumor necrosis factor α (TNF-α), interleukin (IL) 1β, and IL-6. The molecular mechanisms of rosmarinosin A involved the suppression of nuclear factor κB (NF-κB) p65 translocation into the nucleus. Furthermore, rosmarinosin A exhibited anti-inflammatory properties by suppressing the mitogen-activated protein kinase (MAPK) signaling pathway. These findings suggest that rosmarinosin A may exert its anti-inflammatory effects, at least in part, through the modulation of NF-κB and MAPK pathways in LPS-activated macrophages, offering the potential for therapeutic development.