Apparent stratospheric ozone loss rate over Eureka in 1994/95, 1995/96, and 1996/97 inferred from ECC ozonesonde observations

Many ECC-type ozonesondes were launched at the Canadian Arctic Eureka observatory(80°N , 86°W ), one of the most northern stations in the Arctic, during winters from 1993/94 to 2001/02, and the temporal evolutions of the vertical ozone profiles were obtained in detail. The lower stratospheric temperature over Eureka was very low inside the polar vortex and the largest ozone loss was observed in 1999/2000, as reported in a previous paper. Similarly, Eureka was often or persistently inside the vortex in the lower stratosphere(around the 470K isentropic surface level) in the winters of 1994/95, 1995/96, and 1996/97. Very low temperatures were observed inside the vortex in the lower stratosphere over Eureka, as indicated by detection of PSCs by Mie lidar. Observations of tracers(N_2O, total reactive nitrogen species(NOy), and others) inside the vortex during these winters using an ER-2 aircraft and balloons indicated that the effect of air parcel mixing across the vortex edge was minimal, based on the tracer-tracer relationship(e.g., Y. Kondo et al.; J. Geophys. Res., 104D, 8215, 1999). Therefore, significant decreases of the in-travortex ozone mixing ratio in the lower stratosphere were considered to be chemical ozone losses due to chlorine activation of PSCs following diabatic descent. The apparent ozone loss rate inside the vortex over Eureka was estimated for each year. The rates ranged from 0.01 to 0.03ppmv/day, less than that observed in 1999/2000(0.04ppmv/day). The observations were conducted at a single station; however, the apparent ozone loss rate over Eureka inside the vortex each year agrees with loss rates obtained in other studies

Prenylflavonoids isolated from Epimedii Herba show inhibition activity against advanced glycation end-products

Introduction: As inhibitors of advanced glycation end products (AGEs), such as pyridoxamine, significantly inhibit the development of retinopathy and neuropathy in rats with streptozotocin-induced diabetes, treatment with AGE inhibitors is believed to be a potential strategy for the prevention of aging, age-related diseases, and lifestyle-related diseases, including diabetic complications. In the present study, the MeOH extract of Epimedii Herba (EH; aerial parts of Epimedium spp.) was found to inhibit the formation of Nε-(carboxymethyl)lysine (CML) and Nω-(carboxymethyl) arginine (CMA) during the incubation of collagen-derived gelatin with ribose.Materials and methods: EH was purchased from Uchida Wakan-yaku Co., and a MeOH extract was prepared. Several steps of column chromatography purified the extract. Each fraction was tested for inhibitory activity by ELISA using monoclonal antibodies for CML and CMA.Results: After activity-guided fractionation and purification by column chromatography, three new prenylflavonoids [named Koreanoside L (1), Koreanoside E1 (2), and Koreanoside E2 (3)] and 40 known compounds (4–43) were isolated from EH, and their inhibitory effects against CML and CMA formation were tested. Among these, epimedokoreanin B (8), epimedonin E (21), epicornunin B (22), and epicornunin F (24) inhibited the formation of both CML and CMA, with epimedokoreanin B (8) having the most potent inhibitory effect among the isolated compounds. To obtain the structure–activity relationships of 8, the phenolic hydroxy groups of 8 were methylated by trimethylsilyl-diazomethane to afford the partially and completely methylated compounds of 8. Prenyl derivatives of propolis (artepillin C, baccharin, and drupanin) were used in the assay.Discussion: As only 8 showed significant activity among these compounds, the catechol group of the B ring and the two prenyl groups attached to the flavanone skeleton were essential for activity. These data suggest that 8 could prevent the clinical complications of diabetes and age-related diseases by inhibiting AGEs

Involvement of RSK1 activation in malformin-enhanced cellular fibrinolytic activity

Pharmacological interventions to enhance fibrinolysis are effective for treating thrombotic disorders. Utilizing the in vitro U937 cell line-based fibrin degradation assay, we had previously found a cyclic pentapeptide malformin A(1) (MA(1)) as a novel activating compound for cellular fibrinolytic activity. The mechanism by which MA(1) enhances cellular fibrinolytic activity remains unknown. In the present study, we show that RSK1 is a crucial mediator of MA(1)-induced cellular fibrinolysis. Treatment with rhodamine-conjugated MA1 showed that MA(1) localizes mainly in the cytoplasm of U937 cells. Screening with an antibody macroarray revealed that MA(1) induces the phosphorylation of RSK1 at Ser380 in U937 cells. SL0101, an inhibitor of RSK, inhibited MA(1)-induced fibrinolytic activity, and CRISPR/Cas9-mediated knockout of RSK1 but not RSK2 suppressed MA1-enhanced fibrinolysis in U937 cells. Synthetic active MA(1) derivatives also induced the phosphorylation of RSK1. Furthermore, MA(1) treatment stimulated phosphorylation of ERK1/2 and MEK1/2. PD98059, an inhibitor of MEK1/2, inhibited MA(1)-induced phosphorylation of RSK1 and ERK1/2, indicating that MA1 induces the activation of the MEK-ERK-RSK pathway. Moreover, MA(1) upregulated the expression of urokinase-type plasminogen activator (uPA) and increased uPA secretion. These inductions were abrogated in RSK1 knockout cells. These results indicate that RSK1 is a key regulator of MA(1)-induced extracellular fibrinolytic activity