In this study, the long-acting mechanism of reactive species was investigated for enhanced ethanol production of Saccharomyces cerevisiae. The results indicated that short-lifetime active species from gas phase plasma dissolved into various liquid microenvironments with different media (water, buffer, medium, and cells), forming different types and amounts of reactive species in multi-scale microenvironments, such as extracellular reactive nitrogen species, endocellular reactive oxygen and nitrogen species. The sustained elevation of cytoplasm calcium concentration with treatment time depended on the activated calcium channels of Cch1p/Mid1p in cell membrane and Yvc1p in vacuole membrane by these species. Accordingly, the Ca2+ increase promoted the H+-ATPase expression. Consequently, 75.6% ATP hydrolysis induced about 5 fold NADH increase compared with the control. Ultimately, the bioethanol yield increased by 34.2% compared to the control. These results promote the development of atmospheric cold plasma as a promising bio-process enhancement technology for improved target product yields of microbes in fermentation industry.This study investigated the mechanistic functions of CO2 on the pyrolysis of two different biomasses to elucidate the effect of CO2 on syngas formations during pyrolysis. To this end, CO2-assisted pyrolysis of cellulosic biomass (barnyard grass, Echinochloa) and lignin-rich woody biomass (retinispora, Chamaecyparis obtusa) were compared. The confirmed mechanistic effectiveness of CO2 on pyrolysis of biomass was gas phase reactions between CO2 and volatile matters from biomass pyrolysis. Lignin-rich biomass had more CO2 susceptibility, resulting in more enhanced CO formation via the gas phase reactions. To expedite the slow reaction rate of the gas phase reactions during biomass pyrolysis, earth-abundant catalysts (Co/SiO2 and Ni/SiO2) were employed for pyrolysis of two biomass substrates. With Co and Ni catalysts, the syngas formations were 2 and 3 times higher comparing to the pyrolysis of without catalyst. The cumulative formations of syngas from lignin-rich biomass was nearly doubled than that from cellulosic biomass.Carboxypeptidase T (CPT) from Thermoactinomyces vulgaris (EC 3.4.17.18) has a broad substrate specificity, the mechanism of which remains unclear. It cleaves off arginine residues by 10, and lysine residues by 100 times worse than hydrophobic leucine residues despite the presence of negatively charged Asp260 at the bottom of the primary specificity pocket. To study the relationship between the structure and specificity the 3D structure of CPT in complex with the stable transition state analog N-sulfamoyl-l-lysine (SLys) was determined in which the S-atom imitates the sp3-hybridized carbon in the scissile-bond. Crystals grown in microgravity has the symmetry of space group P6322. The present complex structure was compared with the previously reported complex structure of CPT and N-sulfamoyl-L-arginine (SArg). The location/binding of SLys in the active site of CPT very closely resembled that of SArg, and the positively charged N-atom of SLys was at the same position as the corresponding positively charged N-atom of SArg. The SLys complex is stabilized by the hydrogen bond between the nitrogen atom and OH-group of Thr257. The contact areas of the residues Tyr255, Leu211, and Thr262 with SLys were reduced in comparison with the same of SArg. This difference in bonding of SArg and SLys side chains in the primary specificity pocket induces shifts differences within the catalytic center (especially Tyr255-O20 and S18-Arg129 N1 gap) that may influence the enzyme's catalytic reaction. Therefore, this information may be useful for the design of carboxypeptidases with improved selectivity towards Arg/Lys for biotechnological applications. Chemoresistance remains the main obstacle in hepatocellular carcinoma (HCC) therapy. Despite significant advances in HCC therapy, HCC still has a poor prognosis. Thus, there is an urgent need to identify a treatment target to reverse HCC chemotherapy resistance. Platycodon grandiflorus (PG) is a perennial herb that has been used as food and traditional Chinese medicine for thousands of years in Northeast Asia. Platycodin D (PD), a main active triterpenoid saponin found in the root of PG, has been reported to possess anticancer properties in several cancer cell lines, including HCC; however, the reversal effect of this molecule on HCC chemoresistance remains largely unknown. This study aimed to investigate the role and the mechanism of PD-mediated reversal of the histone deacetylase inhibitor (HDACi) resistance in HCC cells. Human HCC cells (HA22T) and HDACi-resistant (HDACi-R) cells were used. Cell viability was measured using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Combi the first time, we showed that PD reversed HDACi resistance in HCC by repressing ERK1/2-mediated cofilin-1 phosphorylation. Thus, PD can potentially be a treatment target to reverse HCC chemotherapy resistance in future therapeutic trials. For the first time, we showed that PD reversed HDACi resistance in HCC by repressing ERK1/2-mediated cofilin-1 phosphorylation. Thus, PD can potentially be a treatment target to reverse HCC chemotherapy resistance in future therapeutic trials.Psoriasis is the most prevalent inflammatory skin disorders, affecting 1-3% of the worldwide population. We previously reported that topical application of methyl 4-(adenin-9-yl)-2-hydroxybutanoate (DZ2002), a reversible S-adenosyl-l-homocysteine hydrolase (SAHH) inhibitor, was a viable treatment in murine psoriatic skin inflammation. In current study, we further explored the mechanisms of DZ2002 on keratinocyte dysfunction and skin infiltration, the key pathogenic events in psoriasis. We conducted genome-wide DNA methylation analysis in skin tissue from imiquimod (IMQ)-induced psoriatic and normal mice, demonstrated that topical administration of DZ2002 directly rectified aberrant DNA methylation pattern in epidermis and dermis of psoriatic skin lesion. Especially, DZ2002 differentially regulated DNA methylation of GATA3 and LCN2 promoters, which maintained keratinocytes differentiation and reduced inflammatory infiltration in psoriatic skin respectively. https://www.selleckchem.com/products/LAQ824(NVP-LAQ824).html In vitro studies in TNF-α/IFN-γ-elicited HaCaT manifested that DZ2002 treatment rectified compromised keratinocyte differentiation via GATA3 enhancement and abated chemokine expression by reducing LCN2 production under inflammatory stimulation.